Nutrient chapter

Chromium

Chromium research collection. Nutritional chromium(III), individual supplement compounds and toxic chromium(VI) are distinct exposures. Human essentiality remains disputed; there is no validated general chromium-status test or established dietary deficiency syndrome. Historical parenteral case reports and experimental low-intake studies retain their specific scope.

87 recorded mechanisms · 5 availability situations · 3 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

The tested picolinate form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.
Chromium(III) picolinate / CrPic → Mouse GLUT4 movement toward or into the cell surface source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
experimental_model
GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
exposure
Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
limitations
Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse 3T3-L1 adipocytes
plain_language
Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response.
primary_references
[chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
tissue_or_cell_type
Cultured adipocyte plasma membrane
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 302–313
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft
### chromium-picolinate-glut4 The tested picolinate form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
Complete structured claim and evidence
AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model.
Rat AMP-activated protein kinase complexes → Insulin-stimulated glucose uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
experimental_model
Hyperinsulinemia model with AMPK silencing
exposure
Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
limitations
Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat L6 skeletal muscle myotubes
plain_language
The glucose-uptake benefit also depended on AMPK in this experiment.
primary_references
[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
tissue_or_cell_type
Cultured muscle plasma membrane and cortical actin
trigger_kind
machinery_impairment Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 406–417
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-required-uptake AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose-uptake benefit also depended on AMPK in this experiment. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
In obese insulin-resistant rats, chromium picolinate increased insulin-stimulated IRS-1 phosphorylation without increasing IRS protein abundance.
Chromium(III) picolinate / CrPic → Rat insulin receptor substrate 1 / Irs1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"}
experimental_model
Three-month supplementation and acute muscle insulin-signaling experiment
exposure
Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups
limitations
Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male JCR:LA-cp obese and lean rats
plain_language
The signaling protein responded more strongly without more of it being present.
primary_references
[chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
tissue_or_cell_type
Vastus lateralis skeletal muscle
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 419–430
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-month supplementation and acute muscle insulin-signaling experiment · source_derived_draft · unverified_draft
### chromium-rat-irs1-phosphorylation In obese insulin-resistant rats, chromium picolinate increased insulin-stimulated IRS-1 phosphorylation without increasing IRS protein abundance. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling protein responded more strongly without more of it being present. organism: Male JCR:LA-cp obese and lean rats tissue_or_cell_type: Vastus lateralis skeletal muscle experimental_model: Three-month supplementation and acute muscle insulin-signaling experiment limitations: Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study. exposure: Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups evidence_span: {"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"} [chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
Complete structured claim and evidence
Obese rats receiving chromium picolinate had lower muscle PTP1B abundance and lower activity after correction for protein content.
Chromium(III) picolinate / CrPic → Rat protein tyrosine phosphatase 1B / Ptpn1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"}
experimental_model
Three-month supplementation and acute muscle insulin-signaling experiment
exposure
Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups
limitations
Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male JCR:LA-cp obese and lean rats
plain_language
A protein that can oppose insulin signaling was reduced in this rat model.
primary_references
[chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
tissue_or_cell_type
Vastus lateralis skeletal muscle
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 445–456
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-month supplementation and acute muscle insulin-signaling experiment · source_derived_draft · unverified_draft
### chromium-rat-ptp1b-response Obese rats receiving chromium picolinate had lower muscle PTP1B abundance and lower activity after correction for protein content. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A protein that can oppose insulin signaling was reduced in this rat model. organism: Male JCR:LA-cp obese and lean rats tissue_or_cell_type: Vastus lateralis skeletal muscle experimental_model: Three-month supplementation and acute muscle insulin-signaling experiment limitations: Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study. exposure: Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups evidence_span: {"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"} [chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
Complete structured claim and evidence
At follow-up, the combined chromium-magnesium group had lower HOMA-IR and glycemic measures than the three other groups in the reported analysis.
Chromium → HOMA-IR estimate of insulin resistance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/38228168.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3", "start_char": 0, "end_char": 1788, "text_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3"}
experimental_model
Four-arm three-month randomized supplementation study; 120 adults
exposure
Chromium, magnesium, combined supplementation or placebo; participants recruited February 2012–February 2015; trial chiCTR-TRC-14004863
limitations
Do not count this automatically as independent replication of the earlier 120-person report. Small groups and baseline sex imbalance limit interpretation. The abstract’s oxidative-marker wording must be read with its p>0.05 combination-versus-single result.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with impaired glucose tolerance and insulin resistance
plain_language
This report included a comparison favoring the combination, while replication and a formal interaction test remain separate questions.
primary_references
[chromium-p38228168] Effects of co-supplementation of chromium and magnesium on metabolic profiles, inflammation, and oxidative stress in impaired glucose tolerance. (2024). https://pubmed.ncbi.nlm.nih.gov/38228168/ DOI: 10.1177/14791641241228156
tissue_or_cell_type
Blood metabolic and oxidative-stress biomarkers
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 601–612
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm three-month randomized supplementation study; 120 adults · source_derived_draft · unverified_draft
### chromium-magnesium-combination-2024 At follow-up, the combined chromium-magnesium group had lower HOMA-IR and glycemic measures than the three other groups in the reported analysis. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This report included a comparison favoring the combination, while replication and a formal interaction test remain separate questions. organism: Human with impaired glucose tolerance and insulin resistance tissue_or_cell_type: Blood metabolic and oxidative-stress biomarkers experimental_model: Four-arm three-month randomized supplementation study; 120 adults limitations: Do not count this automatically as independent replication of the earlier 120-person report. Small groups and baseline sex imbalance limit interpretation. The abstract’s oxidative-marker wording must be read with its p>0.05 combination-versus-single result. exposure: Chromium, magnesium, combined supplementation or placebo; participants recruited February 2012–February 2015; trial chiCTR-TRC-14004863 evidence_span: {"source_cache": "artifacts/chromium-research/38228168.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3", "start_char": 0, "end_char": 1788, "text_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3"} [chromium-p38228168] Effects of co-supplementation of chromium and magnesium on metabolic profiles, inflammation, and oxidative stress in impaired glucose tolerance. (2024). https://pubmed.ncbi.nlm.nih.gov/38228168/ DOI: 10.1177/14791641241228156
Complete structured claim and evidence
The combination trial reported a between-group difference in HbA1c change (p=0.03); HbA1c fell 0.54 percentage points within the active-treatment group.
Chromium(III) picolinate / CrPic → Glycated hemoglobin / HbA1c concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"}
experimental_model
Randomized double-blind placebo-controlled combination trial; 447 enrolled
exposure
600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication
limitations
There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with poorly controlled type 2 diabetes
plain_language
The two-ingredient treatment improved the average long-term glucose marker, but the contribution of each ingredient is unresolved.
primary_references
[chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755
tissue_or_cell_type
HbA1c and fasting glucose
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 692–703
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled combination trial; 447 enrolled · source_derived_draft · unverified_draft
### chromium-biotin-combination-hba1c The combination trial reported a between-group difference in HbA1c change (p=0.03); HbA1c fell 0.54 percentage points within the active-treatment group. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two-ingredient treatment improved the average long-term glucose marker, but the contribution of each ingredient is unresolved. organism: Human with poorly controlled type 2 diabetes tissue_or_cell_type: HbA1c and fasting glucose experimental_model: Randomized double-blind placebo-controlled combination trial; 447 enrolled limitations: There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited. exposure: 600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication evidence_span: {"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"} [chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755
Complete structured claim and evidence
Chromium picolinate did not change the measured hematologic indices, serum iron or ferritin relative to placebo during the training study.
Chromium(III) picolinate / CrPic → Iron-status and hematologic measurements source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9322572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8", "start_char": 0, "end_char": 1869, "text_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8"}
experimental_model
Randomized double-blind supplementation with resistance training; 18 men
exposure
924 µg chromium/day as picolinate versus placebo for 12 weeks; nine men/group
limitations
Small selected population and short follow-up. A negative result does not exclude every interaction in iron-deficient people or other exposures.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human men aged 56–69
plain_language
The proposed iron-depleting effect was not observed in these older men.
primary_references
[chromium-p9322572] Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes. (1997). https://pubmed.ncbi.nlm.nih.gov/9322572/ DOI: 10.1093/ajcn/66.4.944
tissue_or_cell_type
Iron-status and hematologic indices
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 536–547
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind supplementation with resistance training; 18 men · source_derived_draft · unverified_draft
### chromium-human-iron-status-null Chromium picolinate did not change the measured hematologic indices, serum iron or ferritin relative to placebo during the training study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proposed iron-depleting effect was not observed in these older men. organism: Human men aged 56–69 tissue_or_cell_type: Iron-status and hematologic indices experimental_model: Randomized double-blind supplementation with resistance training; 18 men limitations: Small selected population and short follow-up. A negative result does not exclude every interaction in iron-deficient people or other exposures. exposure: 924 µg chromium/day as picolinate versus placebo for 12 weeks; nine men/group evidence_span: {"source_cache": "artifacts/chromium-research/9322572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8", "start_char": 0, "end_char": 1869, "text_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8"} [chromium-p9322572] Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes. (1997). https://pubmed.ncbi.nlm.nih.gov/9322572/ DOI: 10.1093/ajcn/66.4.944
Complete structured claim and evidence
In the 1977 case, intravenous chromium was followed by normalization of the measured glucose-tolerance rate and respiratory quotient after two weeks, with insulin subsequently no longer required.
Chromium → Glucose tolerance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/192066.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c", "start_char": 0, "end_char": 1943, "text_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c"}
experimental_model
Historical long-term parenteral-nutrition case report
exposure
More than five years of parenteral nutrition; 250 µg chromium/day added for two weeks after impaired glucose tolerance and neuropathy
limitations
Single uncontrolled case with complex nutrition and treatment changes. Historical blood/hair reference ranges are not validated current diagnostic thresholds; response to pharmacological chromium does not by itself prove an essential dietary requirement.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human adult patient
plain_language
The patient improved after chromium was added to intravenous nutrition, but a single case cannot establish the general mechanism.
primary_references
[chromium-p192066] Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation, in a patient receiving long-term total parenteral nutrition. (1977). https://pubmed.ncbi.nlm.nih.gov/192066/ DOI: 10.1093/ajcn/30.4.531
tissue_or_cell_type
Systemic glucose utilization and peripheral nerves
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 887–898
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical long-term parenteral-nutrition case report · source_derived_draft · unverified_draft
### chromium-parenteral-glucose-1977 In the 1977 case, intravenous chromium was followed by normalization of the measured glucose-tolerance rate and respiratory quotient after two weeks, with insulin subsequently no longer required. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The patient improved after chromium was added to intravenous nutrition, but a single case cannot establish the general mechanism. organism: Human adult patient tissue_or_cell_type: Systemic glucose utilization and peripheral nerves experimental_model: Historical long-term parenteral-nutrition case report limitations: Single uncontrolled case with complex nutrition and treatment changes. Historical blood/hair reference ranges are not validated current diagnostic thresholds; response to pharmacological chromium does not by itself prove an essential dietary requirement. exposure: More than five years of parenteral nutrition; 250 µg chromium/day added for two weeks after impaired glucose tolerance and neuropathy evidence_span: {"source_cache": "artifacts/chromium-research/192066.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c", "start_char": 0, "end_char": 1943, "text_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c"} [chromium-p192066] Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation, in a patient receiving long-term total parenteral nutrition. (1977). https://pubmed.ncbi.nlm.nih.gov/192066/ DOI: 10.1093/ajcn/30.4.531
Complete structured claim and evidence
The six-month low-chromium diet did not alter glucose responses in glucose- or insulin-tolerance tests relative to the standard diet.
Chromium → Glucose tolerance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/21086001.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd", "start_char": 0, "end_char": 1561, "text_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd"}
experimental_model
Six-month metal-controlled low-chromium feeding experiment
exposure
AIN-93G with no added chromium versus standard diet and supplemental 200 or 1,000 µg Cr/kg
limitations
Low intake is not absolute zero exposure. Lack of abnormality in this rat model challenges essentiality claims but is not by itself a complete human requirement experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Zucker lean rats
plain_language
The rats did not develop the expected glucose-control defect in this carefully controlled model.
primary_references
[chromium-p21086001] Chromium is not an essential trace element for mammals: effects of a "low-chromium" diet. (2011). https://pubmed.ncbi.nlm.nih.gov/21086001/ DOI: 10.1007/s00775-010-0734-y
tissue_or_cell_type
Body composition and glucose/insulin tolerance
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 952–963
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month metal-controlled low-chromium feeding experiment · source_derived_draft · unverified_draft
### chromium-low-diet-glucose-null-2011 The six-month low-chromium diet did not alter glucose responses in glucose- or insulin-tolerance tests relative to the standard diet. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The rats did not develop the expected glucose-control defect in this carefully controlled model. organism: Male Zucker lean rats tissue_or_cell_type: Body composition and glucose/insulin tolerance experimental_model: Six-month metal-controlled low-chromium feeding experiment limitations: Low intake is not absolute zero exposure. Lack of abnormality in this rat model challenges essentiality claims but is not by itself a complete human requirement experiment. exposure: AIN-93G with no added chromium versus standard diet and supplemental 200 or 1,000 µg Cr/kg evidence_span: {"source_cache": "artifacts/chromium-research/21086001.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd", "start_char": 0, "end_char": 1561, "text_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd"} [chromium-p21086001] Chromium is not an essential trace element for mammals: effects of a "low-chromium" diet. (2011). https://pubmed.ncbi.nlm.nih.gov/21086001/ DOI: 10.1007/s00775-010-0734-y
Complete structured claim and evidence
After four months, reported HbA1c values were 8.5%, 7.5% and 6.6% in the placebo, 200 µg/day and 1,000 µg/day groups, respectively.
Chromium(III) picolinate / CrPic → Glycated hemoglobin / HbA1c concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"}
experimental_model
Randomized three-arm supplementation trial; 180 adults
exposure
Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued
limitations
Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with treated type 2 diabetes
plain_language
This trial reported better long-term glucose control with chromium picolinate.
primary_references
[chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
tissue_or_cell_type
HbA1c, glucose, insulin and lipids
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1017–1028
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-arm supplementation trial; 180 adults · source_derived_draft · unverified_draft
### chromium-diabetes-hba1c-positive After four months, reported HbA1c values were 8.5%, 7.5% and 6.6% in the placebo, 200 µg/day and 1,000 µg/day groups, respectively. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This trial reported better long-term glucose control with chromium picolinate. organism: Human with treated type 2 diabetes tissue_or_cell_type: HbA1c, glucose, insulin and lipids experimental_model: Randomized three-arm supplementation trial; 180 adults limitations: Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects. exposure: Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued evidence_span: {"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"} [chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
Complete structured claim and evidence
HbA1c fell by about 0.4 percentage points in all three groups, with no chromium benefit over placebo.
Chromium(III) picolinate / CrPic → Glycated hemoglobin / HbA1c concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16505499.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd1f6a73f70c17bce17b217555cef0c349bd27e8d2bbbe0573b826217039df59", "start_char": 0, "end_char": 1206, "text_sha256": "bd1f6a73f70c17bce17b217555cef0c349bd27e8d2bbbe0573b826217039df59"}
experimental_model
Six-month double-blind randomized placebo-controlled trial
exposure
500 or 1,000 µg Cr/day as picolinate; baseline HbA1c >8% and insulin >50 units/day; per-protocol analysis n=46
limitations
Per-protocol analysis and selected insulin-treated population. This is a clinically relevant null result, not proof that no person can respond.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human obese adults with insulin-treated type 2 diabetes
plain_language
A later trial did not reproduce the earlier glucose-control benefit.
primary_references
[chromium-p16505499] Chromium treatment has no effect in patients with poorly controlled, insulin-treated type 2 diabetes in an obese Western population: a randomized, double-blind, placebo-controlled trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16505499/ DOI: 10.2337/diacare.29.03.06.dc05-1453
tissue_or_cell_type
HbA1c and secondary metabolic endpoints
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1056–1067
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft
### chromium-diabetes-hba1c-null HbA1c fell by about 0.4 percentage points in all three groups, with no chromium benefit over placebo. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A later trial did not reproduce the earlier glucose-control benefit. organism: Human obese adults with insulin-treated type 2 diabetes tissue_or_cell_type: HbA1c and secondary metabolic endpoints experimental_model: Six-month double-blind randomized placebo-controlled trial limitations: Per-protocol analysis and selected insulin-treated population. This is a clinically relevant null result, not proof that no person can respond. exposure: 500 or 1,000 µg Cr/day as picolinate; baseline HbA1c >8% and insulin >50 units/day; per-protocol analysis n=46 evidence_span: {"source_cache": "artifacts/chromium-research/16505499.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd1f6a73f70c17bce17b217555cef0c349bd27e8d2bbbe0573b826217039df59", "start_char": 0, "end_char": 1206, "text_sha256": "bd1f6a73f70c17bce17b217555cef0c349bd27e8d2bbbe0573b826217039df59"} [chromium-p16505499] Chromium treatment has no effect in patients with poorly controlled, insulin-treated type 2 diabetes in an obese Western population: a randomized, double-blind, placebo-controlled trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16505499/ DOI: 10.2337/diacare.29.03.06.dc05-1453
Complete structured claim and evidence
Cr(III) uptake and vascular transfer were nonsaturable across 0.2–20 µmol/L in the perfused rat intestine; the authors interpreted the behavior as passive diffusion.
Trivalent chromium / Cr(III) → Intestinal chromium uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/2778539.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1c3f4249245a1ed57e89179e1f751a537e52fe566de25a9859833895553d2e0e", "start_char": 0, "end_char": 1379, "text_sha256": "1c3f4249245a1ed57e89179e1f751a537e52fe566de25a9859833895553d2e0e"}
experimental_model
Vascularly perfused small-intestine preparation
exposure
Inorganic Cr(III) 0.2–20 µmol/L; chromium-adequate diet before preparation
limitations
Nonsaturability supports passive uptake under this preparation; it does not identify a human transporter or cover all supplement complexes.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat
plain_language
This rat preparation did not show a saturable uptake system over the tested range.
primary_references
[chromium-p2778539] Absorption of inorganic, trivalent chromium from the vascularly perfused rat small intestine. (1989). https://pubmed.ncbi.nlm.nih.gov/2778539/ DOI: 10.1093/jn/119.8.1138
tissue_or_cell_type
Intestinal lumen, wall and vascular perfusate
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 94–105
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vascularly perfused small-intestine preparation · source_derived_draft · unverified_draft
### chromium-rat-intestinal-uptake Cr(III) uptake and vascular transfer were nonsaturable across 0.2–20 µmol/L in the perfused rat intestine; the authors interpreted the behavior as passive diffusion. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This rat preparation did not show a saturable uptake system over the tested range. organism: Rat tissue_or_cell_type: Intestinal lumen, wall and vascular perfusate experimental_model: Vascularly perfused small-intestine preparation limitations: Nonsaturability supports passive uptake under this preparation; it does not identify a human transporter or cover all supplement complexes. exposure: Inorganic Cr(III) 0.2–20 µmol/L; chromium-adequate diet before preparation evidence_span: {"source_cache": "artifacts/chromium-research/2778539.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1c3f4249245a1ed57e89179e1f751a537e52fe566de25a9859833895553d2e0e", "start_char": 0, "end_char": 1379, "text_sha256": "1c3f4249245a1ed57e89179e1f751a537e52fe566de25a9859833895553d2e0e"} [chromium-p2778539] Absorption of inorganic, trivalent chromium from the vascularly perfused rat small intestine. (1989). https://pubmed.ncbi.nlm.nih.gov/2778539/ DOI: 10.1093/jn/119.8.1138
Complete structured claim and evidence
Estimated fractional chromium absorption fell from about 2% at 10 µg/day intake to about 0.5% at 40 µg/day in the study.
Chromium → Intestinal chromium uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/4003325.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e60f6f96d0d74aaba16b4f3e04bdd6c9fe3944c6605df6c4e84180d1987e2013", "start_char": 0, "end_char": 1004, "text_sha256": "e60f6f96d0d74aaba16b4f3e04bdd6c9fe3944c6605df6c4e84180d1987e2013"}
experimental_model
Duplicate-diet collection and absorption estimates in 32 adults
exposure
Seven-day self-selected diets in 10 men and 22 women; approximate intake range 10–40 µg/day for reported absorption relation
limitations
Historical analytical and intake-reference context. A diet below the old suggested intake is not a validated diagnosis of chromium deficiency.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human
plain_language
A greater intake did not translate into a proportionally greater absorbed fraction.
primary_references
[chromium-p4003325] Chromium intake, absorption and excretion of subjects consuming self-selected diets. (1985). https://pubmed.ncbi.nlm.nih.gov/4003325/ DOI: 10.1093/ajcn/41.6.1177
tissue_or_cell_type
Diet and whole-body absorption estimates
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 107–118
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Duplicate-diet collection and absorption estimates in 32 adults · source_derived_draft · unverified_draft
### chromium-human-fractional-absorption Estimated fractional chromium absorption fell from about 2% at 10 µg/day intake to about 0.5% at 40 µg/day in the study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A greater intake did not translate into a proportionally greater absorbed fraction. organism: Human tissue_or_cell_type: Diet and whole-body absorption estimates experimental_model: Duplicate-diet collection and absorption estimates in 32 adults limitations: Historical analytical and intake-reference context. A diet below the old suggested intake is not a validated diagnosis of chromium deficiency. exposure: Seven-day self-selected diets in 10 men and 22 women; approximate intake range 10–40 µg/day for reported absorption relation evidence_span: {"source_cache": "artifacts/chromium-research/4003325.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e60f6f96d0d74aaba16b4f3e04bdd6c9fe3944c6605df6c4e84180d1987e2013", "start_char": 0, "end_char": 1004, "text_sha256": "e60f6f96d0d74aaba16b4f3e04bdd6c9fe3944c6605df6c4e84180d1987e2013"} [chromium-p4003325] Chromium intake, absorption and excretion of subjects consuming self-selected diets. (1985). https://pubmed.ncbi.nlm.nih.gov/4003325/ DOI: 10.1093/ajcn/41.6.1177
Complete structured claim and evidence
Rapid urinary loss accounted for much newly absorbed chromium picolinate; in the human comparison, seven-day retention was similarly low for picolinate and phenylalaninate.
Chromium(III) picolinate / CrPic → Urinary chromium excretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/22814636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6", "start_char": 0, "end_char": 1673, "text_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6"}
experimental_model
Radiolabeled-compound whole-body counting in rats and a human volunteer
exposure
Oral 51Cr-labeled supplement complexes; human intraindividual comparison of picolinate and phenylalaninate
limitations
Human component was a volunteer comparison, not a large population trial. Apparent absorption, absorbed amount before early urinary loss and seven-day retention are different quantities.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat and human; species-specific results retained
plain_language
A compound can enter the body more readily yet leave quickly, without increasing retained chromium.
primary_references
[chromium-p22814636] Bioavailability of chromium(III)-supplements in rats and humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22814636/ DOI: 10.1007/s10534-012-9571-5
tissue_or_cell_type
Intestinal uptake, urine and whole-body retention
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 120–131
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled-compound whole-body counting in rats and a human volunteer · source_derived_draft · unverified_draft
### chromium-picolinate-absorption-retention Rapid urinary loss accounted for much newly absorbed chromium picolinate; in the human comparison, seven-day retention was similarly low for picolinate and phenylalaninate. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A compound can enter the body more readily yet leave quickly, without increasing retained chromium. organism: Rat and human; species-specific results retained tissue_or_cell_type: Intestinal uptake, urine and whole-body retention experimental_model: Radiolabeled-compound whole-body counting in rats and a human volunteer limitations: Human component was a volunteer comparison, not a large population trial. Apparent absorption, absorbed amount before early urinary loss and seven-day retention are different quantities. exposure: Oral 51Cr-labeled supplement complexes; human intraindividual comparison of picolinate and phenylalaninate evidence_span: {"source_cache": "artifacts/chromium-research/22814636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6", "start_char": 0, "end_char": 1673, "text_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6"} [chromium-p22814636] Bioavailability of chromium(III)-supplements in rats and humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22814636/ DOI: 10.1007/s10534-012-9571-5
Complete structured claim and evidence
Apparent absorption in the human comparison was about 0.8–1%, higher than the 0.04–0.24% range across the tested rat complexes.
Chromium(III) picolinate / CrPic → Intestinal chromium uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/22814636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6", "start_char": 0, "end_char": 1673, "text_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6"}
experimental_model
Radiolabeled-compound whole-body counting in rats and a human volunteer
exposure
Oral 51Cr-labeled supplement complexes; human intraindividual comparison of picolinate and phenylalaninate
limitations
Human component was a volunteer comparison, not a large population trial. Apparent absorption, absorbed amount before early urinary loss and seven-day retention are different quantities.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat and human; species-specific results retained
plain_language
Absorption differed between humans and rats; the rat percentage should not be assigned directly to people.
primary_references
[chromium-p22814636] Bioavailability of chromium(III)-supplements in rats and humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22814636/ DOI: 10.1007/s10534-012-9571-5
tissue_or_cell_type
Intestinal uptake, urine and whole-body retention
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 133–144
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled-compound whole-body counting in rats and a human volunteer · source_derived_draft · unverified_draft
### chromium-species-bioavailability Apparent absorption in the human comparison was about 0.8–1%, higher than the 0.04–0.24% range across the tested rat complexes. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Absorption differed between humans and rats; the rat percentage should not be assigned directly to people. organism: Rat and human; species-specific results retained tissue_or_cell_type: Intestinal uptake, urine and whole-body retention experimental_model: Radiolabeled-compound whole-body counting in rats and a human volunteer limitations: Human component was a volunteer comparison, not a large population trial. Apparent absorption, absorbed amount before early urinary loss and seven-day retention are different quantities. exposure: Oral 51Cr-labeled supplement complexes; human intraindividual comparison of picolinate and phenylalaninate evidence_span: {"source_cache": "artifacts/chromium-research/22814636.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6", "start_char": 0, "end_char": 1673, "text_sha256": "392f4199c0cee925fff5f02ee9ce7d12047f9be5d278a55d09da0a3bb707c4b6"} [chromium-p22814636] Bioavailability of chromium(III)-supplements in rats and humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22814636/ DOI: 10.1007/s10534-012-9571-5
Complete structured claim and evidence
Cr(III)-transferrin crystals contained a chromium-loaded closed C-terminal lobe and an open empty N-terminal lobe; two tyrosines, histidine, aspartate and chelating malonate coordinated the metal.
Human serum transferrin / TF → Trivalent chromium / Cr(III) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/32650146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "826e2d7f86ec2016d526ca8a8858db0249f4797aad842189d7f0359b6f375f85", "start_char": 0, "end_char": 1004, "text_sha256": "826e2d7f86ec2016d526ca8a8858db0249f4797aad842189d7f0359b6f375f85"}
experimental_model
X-ray crystallography of chromium-loaded transferrin
exposure
Cr(III)-transferrin crystallized with malonate as the synergistic anion
limitations
Crystal ligands and occupancy depend on preparation; malonate is not evidence that every circulating complex has the same coordination environment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human serum transferrin
plain_language
The iron-carrier protein can bind chromium in a structurally characterized pocket.
primary_references
[chromium-p32650146] X-ray structure of chromium(III)-containing transferrin: First structure of a physiological Cr(III)-binding protein. (2020). https://pubmed.ncbi.nlm.nih.gov/32650146/ DOI: 10.1016/j.jinorgbio.2020.111101
tissue_or_cell_type
Protein crystals
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 146–157
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray crystallography of chromium-loaded transferrin · source_derived_draft · unverified_draft
### chromium-transferrin-crystal Cr(III)-transferrin crystals contained a chromium-loaded closed C-terminal lobe and an open empty N-terminal lobe; two tyrosines, histidine, aspartate and chelating malonate coordinated the metal. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The iron-carrier protein can bind chromium in a structurally characterized pocket. organism: Human serum transferrin tissue_or_cell_type: Protein crystals experimental_model: X-ray crystallography of chromium-loaded transferrin limitations: Crystal ligands and occupancy depend on preparation; malonate is not evidence that every circulating complex has the same coordination environment. exposure: Cr(III)-transferrin crystallized with malonate as the synergistic anion evidence_span: {"source_cache": "artifacts/chromium-research/32650146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "826e2d7f86ec2016d526ca8a8858db0249f4797aad842189d7f0359b6f375f85", "start_char": 0, "end_char": 1004, "text_sha256": "826e2d7f86ec2016d526ca8a8858db0249f4797aad842189d7f0359b6f375f85"} [chromium-p32650146] X-ray structure of chromium(III)-containing transferrin: First structure of a physiological Cr(III)-binding protein. (2020). https://pubmed.ncbi.nlm.nih.gov/32650146/ DOI: 10.1016/j.jinorgbio.2020.111101
Complete structured claim and evidence
Acidic pH promoted rapid Cr(III) release from the weak transferrin site; release from the tighter site was slower and depended on the chelating environment.
Human chromium(III)-loaded transferrin → Chromium release from transferrin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/31669693.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835", "start_char": 0, "end_char": 1635, "text_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835"}
experimental_model
Purified human transferrin release kinetics and soluble receptor interaction
exposure
pH 4.5 and 5.5; weak/tight binding sites; biological chelators and soluble transferrin receptor
limitations
The study establishes release kinetics, not the entire in-vivo pathway. The molecular route from the endosomal lumen to cytosol remains unresolved.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human proteins in vitro
plain_language
Acidification helps release chromium from its carrier, with different behavior at the two sites.
primary_references
[chromium-p31669693] Release of trivalent chromium from serum transferrin is sufficiently rapid to be physiologically relevant. (2020). https://pubmed.ncbi.nlm.nih.gov/31669693/ DOI: 10.1016/j.jinorgbio.2019.110901
tissue_or_cell_type
Endosome-mimicking solution
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 159–170
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human transferrin release kinetics and soluble receptor interaction · source_derived_draft · unverified_draft
### chromium-acidic-release Acidic pH promoted rapid Cr(III) release from the weak transferrin site; release from the tighter site was slower and depended on the chelating environment. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acidification helps release chromium from its carrier, with different behavior at the two sites. organism: Human proteins in vitro tissue_or_cell_type: Endosome-mimicking solution experimental_model: Purified human transferrin release kinetics and soluble receptor interaction limitations: The study establishes release kinetics, not the entire in-vivo pathway. The molecular route from the endosomal lumen to cytosol remains unresolved. exposure: pH 4.5 and 5.5; weak/tight binding sites; biological chelators and soluble transferrin receptor evidence_span: {"source_cache": "artifacts/chromium-research/31669693.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835", "start_char": 0, "end_char": 1635, "text_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835"} [chromium-p31669693] Release of trivalent chromium from serum transferrin is sufficiently rapid to be physiologically relevant. (2020). https://pubmed.ncbi.nlm.nih.gov/31669693/ DOI: 10.1016/j.jinorgbio.2019.110901
Complete structured claim and evidence
Binding of chromium-loaded transferrin to soluble transferrin receptor accelerated chromium release from both sites at acidic pH.
Human transferrin receptor 1 / TFRC → Chromium release from transferrin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/31669693.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835", "start_char": 0, "end_char": 1635, "text_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835"}
experimental_model
Purified human transferrin release kinetics and soluble receptor interaction
exposure
pH 4.5 and 5.5; weak/tight binding sites; biological chelators and soluble transferrin receptor
limitations
The study establishes release kinetics, not the entire in-vivo pathway. The molecular route from the endosomal lumen to cytosol remains unresolved.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human proteins in vitro
plain_language
The receptor changed the carrier’s behavior and helped it release chromium in this assay.
primary_references
[chromium-p31669693] Release of trivalent chromium from serum transferrin is sufficiently rapid to be physiologically relevant. (2020). https://pubmed.ncbi.nlm.nih.gov/31669693/ DOI: 10.1016/j.jinorgbio.2019.110901
tissue_or_cell_type
Endosome-mimicking solution
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 172–183
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human transferrin release kinetics and soluble receptor interaction · source_derived_draft · unverified_draft
### chromium-receptor-accelerated-release Binding of chromium-loaded transferrin to soluble transferrin receptor accelerated chromium release from both sites at acidic pH. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor changed the carrier’s behavior and helped it release chromium in this assay. organism: Human proteins in vitro tissue_or_cell_type: Endosome-mimicking solution experimental_model: Purified human transferrin release kinetics and soluble receptor interaction limitations: The study establishes release kinetics, not the entire in-vivo pathway. The molecular route from the endosomal lumen to cytosol remains unresolved. exposure: pH 4.5 and 5.5; weak/tight binding sites; biological chelators and soluble transferrin receptor evidence_span: {"source_cache": "artifacts/chromium-research/31669693.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835", "start_char": 0, "end_char": 1635, "text_sha256": "bdb962ff7838d36dfbc2cd2df4eed4e07c81ebd824c6e95096c5d7069ec32835"} [chromium-p31669693] Release of trivalent chromium from serum transferrin is sufficiently rapid to be physiologically relevant. (2020). https://pubmed.ncbi.nlm.nih.gov/31669693/ DOI: 10.1016/j.jinorgbio.2019.110901
Complete structured claim and evidence
A human chromium-transferrin conformation formed 5–60 minutes after loading released chromium rapidly at endosomal pH, whereas the slowly formed conformation used in many older assays released it slowly.
Human chromium(III)-loaded transferrin → Chromium release from transferrin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/32088595.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6fd8562bf1ad589db2876f59b6ecd37beda818b8d349e5a42e50d00bb909de0a", "start_char": 0, "end_char": 1535, "text_sha256": "6fd8562bf1ad589db2876f59b6ecd37beda818b8d349e5a42e50d00bb909de0a"}
experimental_model
Time-dependent spectroscopy and release kinetics
exposure
Human apo-transferrin loaded at pH 7.4 in 25 mM bicarbonate; conformations followed over time
limitations
Preparation time changes the protein-metal state. Kinetics alone do not establish essentiality, nutritional benefit or complete cellular delivery.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human and bovine serum transferrin; human conformation series
plain_language
Different preparation states can explain different release-rate measurements without requiring one universal rate.
primary_references
[chromium-p32088595] Significance of conformation changes during the binding and release of chromium(III) from human serum transferrin. (2020). https://pubmed.ncbi.nlm.nih.gov/32088595/ DOI: 10.1016/j.jinorgbio.2020.111040
tissue_or_cell_type
Endosome-mimicking in-vitro solution
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 185–196
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-dependent spectroscopy and release kinetics · source_derived_draft · unverified_draft
### chromium-transferrin-conformation A human chromium-transferrin conformation formed 5–60 minutes after loading released chromium rapidly at endosomal pH, whereas the slowly formed conformation used in many older assays released it slowly. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different preparation states can explain different release-rate measurements without requiring one universal rate. organism: Human and bovine serum transferrin; human conformation series tissue_or_cell_type: Endosome-mimicking in-vitro solution experimental_model: Time-dependent spectroscopy and release kinetics limitations: Preparation time changes the protein-metal state. Kinetics alone do not establish essentiality, nutritional benefit or complete cellular delivery. exposure: Human apo-transferrin loaded at pH 7.4 in 25 mM bicarbonate; conformations followed over time evidence_span: {"source_cache": "artifacts/chromium-research/32088595.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6fd8562bf1ad589db2876f59b6ecd37beda818b8d349e5a42e50d00bb909de0a", "start_char": 0, "end_char": 1535, "text_sha256": "6fd8562bf1ad589db2876f59b6ecd37beda818b8d349e5a42e50d00bb909de0a"} [chromium-p32088595] Significance of conformation changes during the binding and release of chromium(III) from human serum transferrin. (2020). https://pubmed.ncbi.nlm.nih.gov/32088595/ DOI: 10.1016/j.jinorgbio.2020.111040
Complete structured claim and evidence
Insulin stimulated transferrin-associated chromium transport from blood into rat tissues, with liver and kidneys prominent destinations.
Insulin → Delivery of chromium to tissues source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/11472024.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba", "start_char": 0, "end_char": 1224, "text_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba"}
experimental_model
In-vivo chromium tracing with insulin stimulation
exposure
Administered chromium with transferrin transport and insulin comparisons
limitations
Rat tracer findings do not establish a required human insulin-signaling cofactor. Identification of urinary chromodulin was tentative in the indexed abstract.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat
plain_language
An insulin signal changed chromium distribution in this rat experiment.
primary_references
[chromium-p11472024] The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin. (2001). https://pubmed.ncbi.nlm.nih.gov/11472024/ DOI: 10.1007/s007750100238
tissue_or_cell_type
Blood, tissues and urine
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 198–209
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vivo chromium tracing with insulin stimulation · source_derived_draft · unverified_draft
### chromium-insulin-chromium-delivery Insulin stimulated transferrin-associated chromium transport from blood into rat tissues, with liver and kidneys prominent destinations. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An insulin signal changed chromium distribution in this rat experiment. organism: Rat tissue_or_cell_type: Blood, tissues and urine experimental_model: In-vivo chromium tracing with insulin stimulation limitations: Rat tracer findings do not establish a required human insulin-signaling cofactor. Identification of urinary chromodulin was tentative in the indexed abstract. exposure: Administered chromium with transferrin transport and insulin comparisons evidence_span: {"source_cache": "artifacts/chromium-research/11472024.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba", "start_char": 0, "end_char": 1224, "text_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba"} [chromium-p11472024] The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin. (2001). https://pubmed.ncbi.nlm.nih.gov/11472024/ DOI: 10.1007/s007750100238
Complete structured claim and evidence
Insulin-associated urinary chromium loss increased alongside a low-molecular-weight fraction interpreted as probable chromodulin in the rat study.
Insulin → Urinary chromium excretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/11472024.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba", "start_char": 0, "end_char": 1224, "text_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba"}
experimental_model
In-vivo chromium tracing with insulin stimulation
exposure
Administered chromium with transferrin transport and insulin comparisons
limitations
Rat tracer findings do not establish a required human insulin-signaling cofactor. Identification of urinary chromodulin was tentative in the indexed abstract.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat
plain_language
The experiment links insulin exposure to chromium loss, but the identity and physiological role of the urinary complex need qualification.
primary_references
[chromium-p11472024] The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin. (2001). https://pubmed.ncbi.nlm.nih.gov/11472024/ DOI: 10.1007/s007750100238
tissue_or_cell_type
Blood, tissues and urine
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 211–222
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vivo chromium tracing with insulin stimulation · source_derived_draft · unverified_draft
### chromium-insulin-urinary-chromium Insulin-associated urinary chromium loss increased alongside a low-molecular-weight fraction interpreted as probable chromodulin in the rat study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The experiment links insulin exposure to chromium loss, but the identity and physiological role of the urinary complex need qualification. organism: Rat tissue_or_cell_type: Blood, tissues and urine experimental_model: In-vivo chromium tracing with insulin stimulation limitations: Rat tracer findings do not establish a required human insulin-signaling cofactor. Identification of urinary chromodulin was tentative in the indexed abstract. exposure: Administered chromium with transferrin transport and insulin comparisons evidence_span: {"source_cache": "artifacts/chromium-research/11472024.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba", "start_char": 0, "end_char": 1224, "text_sha256": "8760ddbb2dd372b94d71880c6c95441fb876ed2196b4f111988aae1244b3daba"} [chromium-p11472024] The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin. (2001). https://pubmed.ncbi.nlm.nih.gov/11472024/ DOI: 10.1007/s007750100238
Complete structured claim and evidence
The bovine-liver low-molecular-weight isolate contained approximately four Cr(III) ions per peptide, with spectra consistent with carboxylate-supported metal assemblies; one tetranuclear versus two dinuclear assemblies was unresolved.
Bovine liver low-molecular-weight chromium-binding isolate / chromodulin candidate → Trivalent chromium / Cr(III) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9056266.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36be61aa6271d3491a4432d31d5ea6524a059fcc1f1ba1e0acac5f175f711a06", "start_char": 0, "end_char": 791, "text_sha256": "36be61aa6271d3491a4432d31d5ea6524a059fcc1f1ba1e0acac5f175f711a06"}
experimental_model
Isolation and spectroscopy of a bovine-liver chromium-containing peptide fraction
exposure
Spectroscopic characterization of an isolate with approximately four Cr(III) ions per peptide
limitations
The paper interpreted the isolate as naturally occurring; later work questioned whether similar low-molecular-weight species arise during extraction. Exact nuclearity was not resolved by this study.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Bovine liver isolate
plain_language
Researchers isolated a chromium-binding peptide fraction, but its structure and origin inside living cells were not fully settled.
primary_references
[chromium-p9056266] Isolation and characterization of a biologically active chromium oligopeptide from bovine liver. (1997). https://pubmed.ncbi.nlm.nih.gov/9056266/ DOI: 10.1006/abbi.1997.9878
tissue_or_cell_type
Purified fraction outside intact cells
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 224–235
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolation and spectroscopy of a bovine-liver chromium-containing peptide fraction · source_derived_draft · unverified_draft
### chromium-chromodulin-isolate The bovine-liver low-molecular-weight isolate contained approximately four Cr(III) ions per peptide, with spectra consistent with carboxylate-supported metal assemblies; one tetranuclear versus two dinuclear assemblies was unresolved. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Researchers isolated a chromium-binding peptide fraction, but its structure and origin inside living cells were not fully settled. organism: Bovine liver isolate tissue_or_cell_type: Purified fraction outside intact cells experimental_model: Isolation and spectroscopy of a bovine-liver chromium-containing peptide fraction limitations: The paper interpreted the isolate as naturally occurring; later work questioned whether similar low-molecular-weight species arise during extraction. Exact nuclearity was not resolved by this study. exposure: Spectroscopic characterization of an isolate with approximately four Cr(III) ions per peptide evidence_span: {"source_cache": "artifacts/chromium-research/9056266.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36be61aa6271d3491a4432d31d5ea6524a059fcc1f1ba1e0acac5f175f711a06", "start_char": 0, "end_char": 791, "text_sha256": "36be61aa6271d3491a4432d31d5ea6524a059fcc1f1ba1e0acac5f175f711a06"} [chromium-p9056266] Isolation and characterization of a biologically active chromium oligopeptide from bovine liver. (1997). https://pubmed.ncbi.nlm.nih.gov/9056266/ DOI: 10.1006/abbi.1997.9878
Complete structured claim and evidence
Most Cr(III) formed in Cr(VI)-treated cells was associated with high-molecular-mass ligands; cell lysis redistributed chromium into a low-molecular-weight fraction spectroscopically similar to reported chromodulin.
Chromate / chromium(VI) oxyanion → Low-molecular-weight cellular chromium fraction source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/17263387.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35", "start_char": 0, "end_char": 1638, "text_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35"}
experimental_model
X-ray absorption and EPR before and after cell fractionation
exposure
Cr(VI)-treated cells; comparisons with model Cr(III) complexes
limitations
The artifact evidence concerns chromium(VI)-exposed cells and the tested isolation procedures. It does not negate the activity measured when an isolated peptide preparation is added to an enzyme assay.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human A549/HepG2, hamster V79 and mouse C2C12 cells
plain_language
Some apparent chromodulin-like material formed during sample preparation, raising doubts about its identity as a pre-existing cellular signal.
primary_references
[chromium-p17263387] X-ray absorption and EPR spectroscopic studies of the biotransformations of chromium(VI) in mammalian cells. Is chromodulin an artifact of isolation methods? (2007). https://pubmed.ncbi.nlm.nih.gov/17263387/ DOI: 10.1021/ja063792r
tissue_or_cell_type
Intact and lysed cell preparations
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 237–248
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray absorption and EPR before and after cell fractionation · source_derived_draft · unverified_draft
### chromium-chromodulin-isolation-artifact Most Cr(III) formed in Cr(VI)-treated cells was associated with high-molecular-mass ligands; cell lysis redistributed chromium into a low-molecular-weight fraction spectroscopically similar to reported chromodulin. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some apparent chromodulin-like material formed during sample preparation, raising doubts about its identity as a pre-existing cellular signal. organism: Human A549/HepG2, hamster V79 and mouse C2C12 cells tissue_or_cell_type: Intact and lysed cell preparations experimental_model: X-ray absorption and EPR before and after cell fractionation limitations: The artifact evidence concerns chromium(VI)-exposed cells and the tested isolation procedures. It does not negate the activity measured when an isolated peptide preparation is added to an enzyme assay. exposure: Cr(VI)-treated cells; comparisons with model Cr(III) complexes evidence_span: {"source_cache": "artifacts/chromium-research/17263387.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35", "start_char": 0, "end_char": 1638, "text_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35"} [chromium-p17263387] X-ray absorption and EPR spectroscopic studies of the biotransformations of chromium(VI) in mammalian cells. Is chromodulin an artifact of isolation methods? (2007). https://pubmed.ncbi.nlm.nih.gov/17263387/ DOI: 10.1021/ja063792r
Complete structured claim and evidence
The low-molecular-weight chromium-binding preparation bound insulin-activated rat insulin receptor with a reported dissociation constant near 250 pM.
Bovine liver low-molecular-weight chromium-binding isolate / chromodulin candidate → Rat insulin receptor / Insr source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"}
experimental_model
Isolated rat insulin receptor and adipocyte membrane kinase assays
exposure
Insulin activation with added low-molecular-weight chromium-binding material
limitations
Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat receptor; isolated chromium oligopeptide preparation
plain_language
An isolated chromium-binding preparation attached to an activated rat insulin receptor in the assay.
primary_references
[chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
tissue_or_cell_type
Purified receptor and membrane fragments
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 250–261
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat insulin receptor and adipocyte membrane kinase assays · source_derived_draft · unverified_draft
### chromium-chromodulin-insr-binding The low-molecular-weight chromium-binding preparation bound insulin-activated rat insulin receptor with a reported dissociation constant near 250 pM. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An isolated chromium-binding preparation attached to an activated rat insulin receptor in the assay. organism: Rat receptor; isolated chromium oligopeptide preparation tissue_or_cell_type: Purified receptor and membrane fragments experimental_model: Isolated rat insulin receptor and adipocyte membrane kinase assays limitations: Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR. exposure: Insulin activation with added low-molecular-weight chromium-binding material evidence_span: {"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"} [chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
Complete structured claim and evidence
Added chromium oligopeptide enhanced insulin-stimulated receptor tyrosine-kinase activity by up to eightfold in rat adipocyte membrane fragments; no enhancement occurred without insulin.
Bovine liver low-molecular-weight chromium-binding isolate / chromodulin candidate → Insulin receptor tyrosine-kinase activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"}
experimental_model
Isolated rat insulin receptor and adipocyte membrane kinase assays
exposure
Insulin activation with added low-molecular-weight chromium-binding material
limitations
Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat receptor; isolated chromium oligopeptide preparation
plain_language
The preparation amplified an existing insulin signal in this experiment; it did not replace insulin.
primary_references
[chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
tissue_or_cell_type
Purified receptor and membrane fragments
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 263–274
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat insulin receptor and adipocyte membrane kinase assays · source_derived_draft · unverified_draft
### chromium-chromodulin-kinase-amplification Added chromium oligopeptide enhanced insulin-stimulated receptor tyrosine-kinase activity by up to eightfold in rat adipocyte membrane fragments; no enhancement occurred without insulin. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The preparation amplified an existing insulin signal in this experiment; it did not replace insulin. organism: Rat receptor; isolated chromium oligopeptide preparation tissue_or_cell_type: Purified receptor and membrane fragments experimental_model: Isolated rat insulin receptor and adipocyte membrane kinase assays limitations: Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR. exposure: Insulin activation with added low-molecular-weight chromium-binding material evidence_span: {"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"} [chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
Complete structured claim and evidence
The preparation’s ability to enhance insulin-receptor tyrosine-kinase activity depended on its chromium content.
Trivalent chromium / Cr(III) → Bovine liver low-molecular-weight chromium-binding isolate / chromodulin candidate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"}
experimental_model
Isolated rat insulin receptor and adipocyte membrane kinase assays
exposure
Insulin activation with added low-molecular-weight chromium-binding material
limitations
Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat receptor; isolated chromium oligopeptide preparation
plain_language
Removing the preparation’s metal content reduced its assay effect; that does not establish dietary chromium deficiency in humans.
primary_references
[chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
tissue_or_cell_type
Purified receptor and membrane fragments
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 276–287
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat insulin receptor and adipocyte membrane kinase assays · source_derived_draft · unverified_draft
### chromium-chromodulin-metal-dependence The preparation’s ability to enhance insulin-receptor tyrosine-kinase activity depended on its chromium content. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the preparation’s metal content reduced its assay effect; that does not establish dietary chromium deficiency in humans. organism: Rat receptor; isolated chromium oligopeptide preparation tissue_or_cell_type: Purified receptor and membrane fragments experimental_model: Isolated rat insulin receptor and adipocyte membrane kinase assays limitations: Assay activity is distinct from proof of an endogenous human cofactor. The peptide preparation and its cellular origin remain disputed; chromium is not shown to be an obligatory catalytic metal of INSR. exposure: Insulin activation with added low-molecular-weight chromium-binding material evidence_span: {"source_cache": "artifacts/chromium-research/9109644.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283", "start_char": 0, "end_char": 939, "text_sha256": "23e955cef071c135f3935f440f4e333d49f494f004ceb22574df717c86bb7283"} [chromium-p9109644] Chromium oligopeptide activates insulin receptor tyrosine kinase activity. (1997). https://pubmed.ncbi.nlm.nih.gov/9109644/ DOI: 10.1021/bi963154t
Complete structured claim and evidence
The isolate increased membrane phosphotyrosine-phosphatase activity in proportion to the amount added, while the isolate itself had no intrinsic phosphatase activity.
Bovine liver low-molecular-weight chromium-binding isolate / chromodulin candidate → Adipocyte membrane phosphotyrosine phosphatases (identity unresolved) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/8841143.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04928cdcbe3e2a282fa43f6a987d1846c6a4e882a6834542b19578b43f8f8322", "start_char": 0, "end_char": 942, "text_sha256": "04928cdcbe3e2a282fa43f6a987d1846c6a4e882a6834542b19578b43f8f8322"}
experimental_model
Membrane phosphatase kinetics and inhibitor profiling
exposure
Added low-molecular-weight chromium-binding preparation
limitations
The phosphatase was not molecularly identified. Inhibitor behavior suggested similarity to PTP1A′ or PTP1B but does not justify assigning this result to a specific gene. Activation here is not proof of universal PTP1B inhibition.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Bovine liver isolate; adipocyte membranes
plain_language
This experiment increased a phosphatase activity; the exact enzyme identity remained unresolved.
primary_references
[chromium-p8841143] A biologically active form of chromium may activate a membrane phosphotyrosine phosphatase (PTP). (1996). https://pubmed.ncbi.nlm.nih.gov/8841143/ DOI: 10.1021/bi960328y
tissue_or_cell_type
Cell-membrane enzyme preparation
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 289–300
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Membrane phosphatase kinetics and inhibitor profiling · source_derived_draft · unverified_draft
### chromium-membrane-phosphatase-activation The isolate increased membrane phosphotyrosine-phosphatase activity in proportion to the amount added, while the isolate itself had no intrinsic phosphatase activity. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This experiment increased a phosphatase activity; the exact enzyme identity remained unresolved. organism: Bovine liver isolate; adipocyte membranes tissue_or_cell_type: Cell-membrane enzyme preparation experimental_model: Membrane phosphatase kinetics and inhibitor profiling limitations: The phosphatase was not molecularly identified. Inhibitor behavior suggested similarity to PTP1A′ or PTP1B but does not justify assigning this result to a specific gene. Activation here is not proof of universal PTP1B inhibition. exposure: Added low-molecular-weight chromium-binding preparation evidence_span: {"source_cache": "artifacts/chromium-research/8841143.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "04928cdcbe3e2a282fa43f6a987d1846c6a4e882a6834542b19578b43f8f8322", "start_char": 0, "end_char": 942, "text_sha256": "04928cdcbe3e2a282fa43f6a987d1846c6a4e882a6834542b19578b43f8f8322"} [chromium-p8841143] A biologically active form of chromium may activate a membrane phosphotyrosine phosphatase (PTP). (1996). https://pubmed.ncbi.nlm.nih.gov/8841143/ DOI: 10.1021/bi960328y
Complete structured claim and evidence
The tested chloride form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.
Chromium(III) chloride → Mouse GLUT4 movement toward or into the cell surface source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
experimental_model
GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
exposure
Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
limitations
Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse 3T3-L1 adipocytes
plain_language
Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response.
primary_references
[chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
tissue_or_cell_type
Cultured adipocyte plasma membrane
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 315–326
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft
### chromium-chloride-glut4 The tested chloride form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium exposure moved glucose transporters closer to the surface, but insulin was still needed for the functional response. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
Complete structured claim and evidence
Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit.
Chromium(III) picolinate / CrPic → Insulin-stimulated glucose uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
experimental_model
GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
exposure
Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
limitations
Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse 3T3-L1 adipocytes
plain_language
Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism.
primary_references
[chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
tissue_or_cell_type
Cultured adipocyte plasma membrane
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 328–339
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft
### chromium-cholesterol-dependent-uptake Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
Complete structured claim and evidence
Chromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps.
Chromium(III) picolinate / CrPic → Insulin receptor autophosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
experimental_model
GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
exposure
Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
limitations
Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse 3T3-L1 adipocytes
plain_language
The transporter effect did not require a bigger response in the insulin-signaling measurements tested here.
primary_references
[chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
tissue_or_cell_type
Cultured adipocyte plasma membrane
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 341–352
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft
### chromium-proximal-signaling-not-amplified Chromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter effect did not require a bigger response in the insulin-signaling measurements tested here. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
Complete structured claim and evidence
Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment.
Chromium(III) picolinate / CrPic → Rat AMP-activated protein kinase complexes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
experimental_model
Hyperinsulinemia model with AMPK silencing
exposure
Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
limitations
Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat L6 skeletal muscle myotubes
plain_language
The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling.
primary_references
[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
tissue_or_cell_type
Cultured muscle plasma membrane and cortical actin
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 354–365
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-response Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
Chromium picolinate protected hyperinsulinemic L6 myotubes against excess membrane cholesterol.
Chromium(III) picolinate / CrPic → Plasma-membrane cholesterol content source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
experimental_model
Hyperinsulinemia model with AMPK silencing
exposure
Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
limitations
Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat L6 skeletal muscle myotubes
plain_language
The treatment prevented a membrane-lipid change associated with insulin resistance in this model.
primary_references
[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
tissue_or_cell_type
Cultured muscle plasma membrane and cortical actin
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 367–378
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-membrane-cholesterol-protection Chromium picolinate protected hyperinsulinemic L6 myotubes against excess membrane cholesterol. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treatment prevented a membrane-lipid change associated with insulin resistance in this model. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
Chromium picolinate protected L6 myotubes from hyperinsulinemia-associated cortical filamentous-actin loss.
Chromium(III) picolinate / CrPic → Cortical filamentous-actin integrity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
experimental_model
Hyperinsulinemia model with AMPK silencing
exposure
Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
limitations
Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat L6 skeletal muscle myotubes
plain_language
The cell’s supporting actin structure was better preserved under the tested conditions.
primary_references
[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
tissue_or_cell_type
Cultured muscle plasma membrane and cortical actin
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 380–391
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-cortical-actin-protection Chromium picolinate protected L6 myotubes from hyperinsulinemia-associated cortical filamentous-actin loss. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell’s supporting actin structure was better preserved under the tested conditions. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes.
Rat AMP-activated protein kinase complexes → Rat GLUT4 translocation to the cell surface source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
experimental_model
Hyperinsulinemia model with AMPK silencing
exposure
Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
limitations
Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat L6 skeletal muscle myotubes
plain_language
When AMPK was depleted, this transporter response to chromium picolinate was lost.
primary_references
[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
tissue_or_cell_type
Cultured muscle plasma membrane and cortical actin
trigger_kind
machinery_impairment Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 393–404
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-required-glut4 AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: When AMPK was depleted, this transporter response to chromium picolinate was lost. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
Chromium picolinate increased insulin-stimulated PI3K activity in muscle from the obese rats without increasing PI3K protein abundance.
Chromium(III) picolinate / CrPic → Rat phosphatidylinositol 3-kinase complexes (isoform unresolved) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"}
experimental_model
Three-month supplementation and acute muscle insulin-signaling experiment
exposure
Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups
limitations
Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male JCR:LA-cp obese and lean rats
plain_language
Another downstream insulin-signaling step became more active.
primary_references
[chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
tissue_or_cell_type
Vastus lateralis skeletal muscle
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 432–443
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-month supplementation and acute muscle insulin-signaling experiment · source_derived_draft · unverified_draft
### chromium-rat-pi3k-activity Chromium picolinate increased insulin-stimulated PI3K activity in muscle from the obese rats without increasing PI3K protein abundance. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another downstream insulin-signaling step became more active. organism: Male JCR:LA-cp obese and lean rats tissue_or_cell_type: Vastus lateralis skeletal muscle experimental_model: Three-month supplementation and acute muscle insulin-signaling experiment limitations: Model-specific supplementation. Lower phosphatase protein and activity do not prove direct chromium binding to PTP1B. Different results from cultured adipocytes are contextual, not a reason to erase either study. exposure: Chromium picolinate supplying approximately 80 µg Cr/kg/day; small obese and lean treatment groups evidence_span: {"source_cache": "artifacts/chromium-research/16424121.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119", "start_char": 0, "end_char": 1734, "text_sha256": "b0fa1d0917ec9cf4f3d309f2e9eb0e2b498e083ed1ff881b8f8df94a3cbe8119"} [chromium-p16424121] Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. (2006). https://pubmed.ncbi.nlm.nih.gov/16424121/ DOI: 10.1093/jn/136.2.415
Complete structured claim and evidence
Chromium picolinate increased plasma-membrane CD36 localization in 3T3-L1 adipocytes; combining it with insulin did not produce additive CD36 translocation.
Chromium(III) picolinate / CrPic → Mouse CD36 movement to the cell surface source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/20721637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f", "start_char": 0, "end_char": 1671, "text_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f"}
experimental_model
Transporter localization and substrate-uptake assays
exposure
Insulin, chromium picolinate and wortmannin comparisons
limitations
Membrane localization is not equivalent to transporter activity. CD36 trafficking responses to insulin and chromium were not additive; results do not show a general increase in beneficial fatty-acid disposal.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse 3T3-L1 adipocytes
plain_language
Chromium affected a fatty-acid transporter as well as GLUT4, with a different response pattern.
primary_references
[chromium-p20721637] Insulin and chromium picolinate induce translocation of CD36 to the plasma membrane through different signaling pathways in 3T3-L1 adipocytes, and with a differential functionality of the CD36. (2011). https://pubmed.ncbi.nlm.nih.gov/20721637/ DOI: 10.1007/s12011-010-8809-8
tissue_or_cell_type
Plasma membrane
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 458–469
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter localization and substrate-uptake assays · source_derived_draft · unverified_draft
### chromium-cd36-trafficking Chromium picolinate increased plasma-membrane CD36 localization in 3T3-L1 adipocytes; combining it with insulin did not produce additive CD36 translocation. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium affected a fatty-acid transporter as well as GLUT4, with a different response pattern. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Plasma membrane experimental_model: Transporter localization and substrate-uptake assays limitations: Membrane localization is not equivalent to transporter activity. CD36 trafficking responses to insulin and chromium were not additive; results do not show a general increase in beneficial fatty-acid disposal. exposure: Insulin, chromium picolinate and wortmannin comparisons evidence_span: {"source_cache": "artifacts/chromium-research/20721637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f", "start_char": 0, "end_char": 1671, "text_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f"} [chromium-p20721637] Insulin and chromium picolinate induce translocation of CD36 to the plasma membrane through different signaling pathways in 3T3-L1 adipocytes, and with a differential functionality of the CD36. (2011). https://pubmed.ncbi.nlm.nih.gov/20721637/ DOI: 10.1007/s12011-010-8809-8
Complete structured claim and evidence
Glycated transferrin retained two chromium-binding equivalents but had altered spectroscopic behavior and greatly reduced chromium delivery in rats.
Experimentally glycated transferrin (species not specified in indexed abstract) → Delivery of chromium to tissues source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/27592288.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541c9ba554cad6d899569dc16cdd68b1125542e2df006cb50db19f66d6e78d09", "start_char": 0, "end_char": 1460, "text_sha256": "541c9ba554cad6d899569dc16cdd68b1125542e2df006cb50db19f66d6e78d09"}
experimental_model
Transferrin incubation, metal binding and rat delivery experiments
exposure
Transferrin stored at 37°C with or without glucose before chromium binding and delivery assays
limitations
Protein storage itself altered binding. The glycated-protein result does not establish chromium deficiency in human diabetes or a treatment response.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Purified transferrin and rat in-vivo transport
plain_language
A carrier can still bind the metal yet distribute it less effectively.
primary_references
[chromium-p27592288] The effects of the glycation of transferrin on chromium binding and the transport and distribution of chromium in vivo. (2016). https://pubmed.ncbi.nlm.nih.gov/27592288/ DOI: 10.1016/j.jinorgbio.2016.08.008
tissue_or_cell_type
Carrier protein and systemic chromium distribution
trigger_kind
machinery_impairment Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 471–482
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transferrin incubation, metal binding and rat delivery experiments · source_derived_draft · unverified_draft
### chromium-glycated-transferrin-delivery Glycated transferrin retained two chromium-binding equivalents but had altered spectroscopic behavior and greatly reduced chromium delivery in rats. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A carrier can still bind the metal yet distribute it less effectively. organism: Purified transferrin and rat in-vivo transport tissue_or_cell_type: Carrier protein and systemic chromium distribution experimental_model: Transferrin incubation, metal binding and rat delivery experiments limitations: Protein storage itself altered binding. The glycated-protein result does not establish chromium deficiency in human diabetes or a treatment response. exposure: Transferrin stored at 37°C with or without glucose before chromium binding and delivery assays evidence_span: {"source_cache": "artifacts/chromium-research/27592288.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541c9ba554cad6d899569dc16cdd68b1125542e2df006cb50db19f66d6e78d09", "start_char": 0, "end_char": 1460, "text_sha256": "541c9ba554cad6d899569dc16cdd68b1125542e2df006cb50db19f66d6e78d09"} [chromium-p27592288] The effects of the glycation of transferrin on chromium binding and the transport and distribution of chromium in vivo. (2016). https://pubmed.ncbi.nlm.nih.gov/27592288/ DOI: 10.1016/j.jinorgbio.2016.08.008
Complete structured claim and evidence
Chromium supplementation raised tissue chromium less strongly in iron-deficient rats than in rats with adequate iron.
Iron → Delivery of chromium to tissues source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/29173471.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e", "start_char": 0, "end_char": 1448, "text_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e"}
experimental_model
Six-week factorial chromium/iron feeding study
exposure
Iron at 10% versus 100% of the study reference level; chromium propionate at 1, 50 or 500 mg Cr/kg diet
limitations
Very high chromium doses in an animal experiment. Changes do not establish a recommended human ratio, a chromium rescue for anemia or a universal competition rule.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Female Wistar rats
plain_language
Low iron did not simply free more carrier space and increase chromium accumulation.
primary_references
[chromium-p29173471] The combined effect of supplementary Cr(III) propionate complex and iron deficiency on the chromium and iron status in female rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29173471/ DOI: 10.1016/j.jtemb.2017.10.010
tissue_or_cell_type
Tissue metals and hematologic indices
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 484–495
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-week factorial chromium/iron feeding study · source_derived_draft · unverified_draft
### chromium-iron-deficiency-chromium Chromium supplementation raised tissue chromium less strongly in iron-deficient rats than in rats with adequate iron. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low iron did not simply free more carrier space and increase chromium accumulation. organism: Female Wistar rats tissue_or_cell_type: Tissue metals and hematologic indices experimental_model: Six-week factorial chromium/iron feeding study limitations: Very high chromium doses in an animal experiment. Changes do not establish a recommended human ratio, a chromium rescue for anemia or a universal competition rule. exposure: Iron at 10% versus 100% of the study reference level; chromium propionate at 1, 50 or 500 mg Cr/kg diet evidence_span: {"source_cache": "artifacts/chromium-research/29173471.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e", "start_char": 0, "end_char": 1448, "text_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e"} [chromium-p29173471] The combined effect of supplementary Cr(III) propionate complex and iron deficiency on the chromium and iron status in female rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29173471/ DOI: 10.1016/j.jtemb.2017.10.010
Complete structured claim and evidence
High chromium-propionate supplementation did not deepen the measured adverse iron-status and hematologic changes from iron restriction.
Trinuclear oxo chromium(III) propionate complex / Cr3 → Iron-status and hematologic measurements source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/29173471.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e", "start_char": 0, "end_char": 1448, "text_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e"}
experimental_model
Six-week factorial chromium/iron feeding study
exposure
Iron at 10% versus 100% of the study reference level; chromium propionate at 1, 50 or 500 mg Cr/kg diet
limitations
Very high chromium doses in an animal experiment. Changes do not establish a recommended human ratio, a chromium rescue for anemia or a universal competition rule.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Female Wistar rats
plain_language
This animal experiment did not show the predicted worsening of iron status.
primary_references
[chromium-p29173471] The combined effect of supplementary Cr(III) propionate complex and iron deficiency on the chromium and iron status in female rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29173471/ DOI: 10.1016/j.jtemb.2017.10.010
tissue_or_cell_type
Tissue metals and hematologic indices
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 497–508
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-week factorial chromium/iron feeding study · source_derived_draft · unverified_draft
### chromium-iron-deficiency-not-worsened High chromium-propionate supplementation did not deepen the measured adverse iron-status and hematologic changes from iron restriction. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This animal experiment did not show the predicted worsening of iron status. organism: Female Wistar rats tissue_or_cell_type: Tissue metals and hematologic indices experimental_model: Six-week factorial chromium/iron feeding study limitations: Very high chromium doses in an animal experiment. Changes do not establish a recommended human ratio, a chromium rescue for anemia or a universal competition rule. exposure: Iron at 10% versus 100% of the study reference level; chromium propionate at 1, 50 or 500 mg Cr/kg diet evidence_span: {"source_cache": "artifacts/chromium-research/29173471.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e", "start_char": 0, "end_char": 1448, "text_sha256": "9de0b60d39b67304da3d1042ebc5f1ed5622a5675e6a0cda4c531bf64249ef2e"} [chromium-p29173471] The combined effect of supplementary Cr(III) propionate complex and iron deficiency on the chromium and iron status in female rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29173471/ DOI: 10.1016/j.jtemb.2017.10.010
Complete structured claim and evidence
High dietary iron reduced serum, liver and kidney chromium concentrations in the study.
Iron → Circulating chromium concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/29164513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b", "start_char": 0, "end_char": 2450, "text_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b"}
experimental_model
Factorial six-group iron-excess/chromium feeding experiment
exposure
Iron 45 versus 180 mg/kg diet; chromium propionate 1, 50 or 500 mg Cr/kg diet; six animals/group
limitations
High-dose animal study. The direction changed with background iron; do not extrapolate a universal nutrient antagonism or human dose ratio.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Female Wistar rats
plain_language
Excess iron changed chromium distribution under these rat feeding conditions.
primary_references
[chromium-p29164513] The Combined Effects of Iron Excess in the Diet and Chromium(III) Supplementation on the Iron and Chromium Status in Female Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29164513/ DOI: 10.1007/s12011-017-1203-z
tissue_or_cell_type
Serum, liver and kidney metals
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 510–521
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Factorial six-group iron-excess/chromium feeding experiment · source_derived_draft · unverified_draft
### chromium-iron-excess-chromium High dietary iron reduced serum, liver and kidney chromium concentrations in the study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess iron changed chromium distribution under these rat feeding conditions. organism: Female Wistar rats tissue_or_cell_type: Serum, liver and kidney metals experimental_model: Factorial six-group iron-excess/chromium feeding experiment limitations: High-dose animal study. The direction changed with background iron; do not extrapolate a universal nutrient antagonism or human dose ratio. exposure: Iron 45 versus 180 mg/kg diet; chromium propionate 1, 50 or 500 mg Cr/kg diet; six animals/group evidence_span: {"source_cache": "artifacts/chromium-research/29164513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b", "start_char": 0, "end_char": 2450, "text_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b"} [chromium-p29164513] The Combined Effects of Iron Excess in the Diet and Chromium(III) Supplementation on the Iron and Chromium Status in Female Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29164513/ DOI: 10.1007/s12011-017-1203-z
Complete structured claim and evidence
Chromium supplementation reduced kidney iron with adequate dietary iron, but increasing chromium raised kidney iron when the background diet was iron-excessive.
Trinuclear oxo chromium(III) propionate complex / Cr3 → Renal iron concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/29164513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b", "start_char": 0, "end_char": 2450, "text_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b"}
experimental_model
Factorial six-group iron-excess/chromium feeding experiment
exposure
Iron 45 versus 180 mg/kg diet; chromium propionate 1, 50 or 500 mg Cr/kg diet; six animals/group
limitations
High-dose animal study. The direction changed with background iron; do not extrapolate a universal nutrient antagonism or human dose ratio.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Female Wistar rats
plain_language
The same supplement did not have one fixed effect on kidney iron.
primary_references
[chromium-p29164513] The Combined Effects of Iron Excess in the Diet and Chromium(III) Supplementation on the Iron and Chromium Status in Female Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29164513/ DOI: 10.1007/s12011-017-1203-z
tissue_or_cell_type
Serum, liver and kidney metals
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 523–534
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Factorial six-group iron-excess/chromium feeding experiment · source_derived_draft · unverified_draft
### chromium-renal-iron-context Chromium supplementation reduced kidney iron with adequate dietary iron, but increasing chromium raised kidney iron when the background diet was iron-excessive. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same supplement did not have one fixed effect on kidney iron. organism: Female Wistar rats tissue_or_cell_type: Serum, liver and kidney metals experimental_model: Factorial six-group iron-excess/chromium feeding experiment limitations: High-dose animal study. The direction changed with background iron; do not extrapolate a universal nutrient antagonism or human dose ratio. exposure: Iron 45 versus 180 mg/kg diet; chromium propionate 1, 50 or 500 mg Cr/kg diet; six animals/group evidence_span: {"source_cache": "artifacts/chromium-research/29164513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b", "start_char": 0, "end_char": 2450, "text_sha256": "4d99145cb86f4110fd0087f9162fa057d87b445b9bc6a60c6467bb310f5e300b"} [chromium-p29164513] The Combined Effects of Iron Excess in the Diet and Chromium(III) Supplementation on the Iron and Chromium Status in Female Rats. (2018). https://pubmed.ncbi.nlm.nih.gov/29164513/ DOI: 10.1007/s12011-017-1203-z
Complete structured claim and evidence
Chromium picolinate did not alter the training-associated changes in total iron-binding capacity or transferrin saturation.
Chromium(III) picolinate / CrPic → Transferrin saturation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9322572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8", "start_char": 0, "end_char": 1869, "text_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8"}
experimental_model
Randomized double-blind supplementation with resistance training; 18 men
exposure
924 µg chromium/day as picolinate versus placebo for 12 weeks; nine men/group
limitations
Small selected population and short follow-up. A negative result does not exclude every interaction in iron-deficient people or other exposures.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human men aged 56–69
plain_language
Sharing carrier chemistry did not translate into a detectable adverse iron-transport effect in this trial.
primary_references
[chromium-p9322572] Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes. (1997). https://pubmed.ncbi.nlm.nih.gov/9322572/ DOI: 10.1093/ajcn/66.4.944
tissue_or_cell_type
Iron-status and hematologic indices
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 549–560
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind supplementation with resistance training; 18 men · source_derived_draft · unverified_draft
### chromium-human-transferrin-saturation-null Chromium picolinate did not alter the training-associated changes in total iron-binding capacity or transferrin saturation. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sharing carrier chemistry did not translate into a detectable adverse iron-transport effect in this trial. organism: Human men aged 56–69 tissue_or_cell_type: Iron-status and hematologic indices experimental_model: Randomized double-blind supplementation with resistance training; 18 men limitations: Small selected population and short follow-up. A negative result does not exclude every interaction in iron-deficient people or other exposures. exposure: 924 µg chromium/day as picolinate versus placebo for 12 weeks; nine men/group evidence_span: {"source_cache": "artifacts/chromium-research/9322572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8", "start_char": 0, "end_char": 1869, "text_sha256": "767fd4144862b2bbc3bf416541442924fc69da030435898b1e6843dba8e35dc8"} [chromium-p9322572] Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes. (1997). https://pubmed.ncbi.nlm.nih.gov/9322572/ DOI: 10.1093/ajcn/66.4.944
Complete structured claim and evidence
The chromium-plus-magnesium group had lower fasting glucose, fasting insulin and the reported insulin-resistance index than its own baseline; the individual-treatment groups lacked significant within-group changes.
Chromium → Calculated insulin-resistance index (formula not verified) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"}
experimental_model
Four-arm randomized supplementation study; 120 insulin-resistant adults
exposure
Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo
limitations
The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human
plain_language
The combination showed a signal in this trial, but comparing which groups reached significance does not by itself prove synergy.
primary_references
[chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
tissue_or_cell_type
Blood measures and activated T lymphocytes
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 562–573
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation study; 120 insulin-resistant adults · source_derived_draft · unverified_draft
### chromium-magnesium-combination-2016 The chromium-plus-magnesium group had lower fasting glucose, fasting insulin and the reported insulin-resistance index than its own baseline; the individual-treatment groups lacked significant within-group changes. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination showed a signal in this trial, but comparing which groups reached significance does not by itself prove synergy. organism: Human tissue_or_cell_type: Blood measures and activated T lymphocytes experimental_model: Four-arm randomized supplementation study; 120 insulin-resistant adults limitations: The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved. exposure: Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo evidence_span: {"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"} [chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
Complete structured claim and evidence
GLUT4 mRNA increased 2.9-fold from baseline in activated T lymphocytes in the combined-treatment group.
Chromium → Human glucose transporter 4 / SLC2A4 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"}
experimental_model
Four-arm randomized supplementation study; 120 insulin-resistant adults
exposure
Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo
limitations
The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human
plain_language
The combination changed a transporter’s gene-expression measurement in immune cells.
primary_references
[chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
tissue_or_cell_type
Blood measures and activated T lymphocytes
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 575–586
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation study; 120 insulin-resistant adults · source_derived_draft · unverified_draft
### chromium-magnesium-glut4-transcript GLUT4 mRNA increased 2.9-fold from baseline in activated T lymphocytes in the combined-treatment group. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination changed a transporter’s gene-expression measurement in immune cells. organism: Human tissue_or_cell_type: Blood measures and activated T lymphocytes experimental_model: Four-arm randomized supplementation study; 120 insulin-resistant adults limitations: The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved. exposure: Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo evidence_span: {"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"} [chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
Complete structured claim and evidence
GSK3β mRNA decreased 2.2-fold from baseline in activated T lymphocytes in the combined-treatment group.
Chromium → Human glycogen synthase kinase 3 beta / GSK3B source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"}
experimental_model
Four-arm randomized supplementation study; 120 insulin-resistant adults
exposure
Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo
limitations
The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human
plain_language
A separate regulator of insulin-related metabolism showed lower gene expression in those immune cells.
primary_references
[chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
tissue_or_cell_type
Blood measures and activated T lymphocytes
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 588–599
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation study; 120 insulin-resistant adults · source_derived_draft · unverified_draft
### chromium-magnesium-gsk3-transcript GSK3β mRNA decreased 2.2-fold from baseline in activated T lymphocytes in the combined-treatment group. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate regulator of insulin-related metabolism showed lower gene expression in those immune cells. organism: Human tissue_or_cell_type: Blood measures and activated T lymphocytes experimental_model: Four-arm randomized supplementation study; 120 insulin-resistant adults limitations: The abstract principally reports within-group changes, which alone do not establish a between-group interaction. T-lymphocyte mRNA is not skeletal-muscle transporter activity. Possible participant overlap with later reports is not resolved. exposure: Three months: chromium 160 µg/day, magnesium 200 mg/day, both, or placebo evidence_span: {"source_cache": "artifacts/chromium-research/27702717.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e", "start_char": 0, "end_char": 1556, "text_sha256": "5a066f8a51a4f0d4b33648166fc5bae559c5132e1ae35d65347c178359447d7e"} [chromium-p27702717] Combined chromium and magnesium decreases insulin resistance more effectively than either alone. (2016). https://pubmed.ncbi.nlm.nih.gov/27702717/ DOI: 10.6133/apjcn.092015.48
Complete structured claim and evidence
The combined-treatment group had higher HDL cholesterol than the other groups in the reported analysis.
Chromium → HDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/38228168.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3", "start_char": 0, "end_char": 1788, "text_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3"}
experimental_model
Four-arm three-month randomized supplementation study; 120 adults
exposure
Chromium, magnesium, combined supplementation or placebo; participants recruited February 2012–February 2015; trial chiCTR-TRC-14004863
limitations
Do not count this automatically as independent replication of the earlier 120-person report. Small groups and baseline sex imbalance limit interpretation. The abstract’s oxidative-marker wording must be read with its p>0.05 combination-versus-single result.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with impaired glucose tolerance and insulin resistance
plain_language
The trial also reported a lipid change with the combination.
primary_references
[chromium-p38228168] Effects of co-supplementation of chromium and magnesium on metabolic profiles, inflammation, and oxidative stress in impaired glucose tolerance. (2024). https://pubmed.ncbi.nlm.nih.gov/38228168/ DOI: 10.1177/14791641241228156
tissue_or_cell_type
Blood metabolic and oxidative-stress biomarkers
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 614–625
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm three-month randomized supplementation study; 120 adults · source_derived_draft · unverified_draft
### chromium-magnesium-hdl The combined-treatment group had higher HDL cholesterol than the other groups in the reported analysis. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial also reported a lipid change with the combination. organism: Human with impaired glucose tolerance and insulin resistance tissue_or_cell_type: Blood metabolic and oxidative-stress biomarkers experimental_model: Four-arm three-month randomized supplementation study; 120 adults limitations: Do not count this automatically as independent replication of the earlier 120-person report. Small groups and baseline sex imbalance limit interpretation. The abstract’s oxidative-marker wording must be read with its p>0.05 combination-versus-single result. exposure: Chromium, magnesium, combined supplementation or placebo; participants recruited February 2012–February 2015; trial chiCTR-TRC-14004863 evidence_span: {"source_cache": "artifacts/chromium-research/38228168.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3", "start_char": 0, "end_char": 1788, "text_sha256": "b4c183c056f1fb256f33169031be43fd7c78d14601c85ea237e46987c7923be3"} [chromium-p38228168] Effects of co-supplementation of chromium and magnesium on metabolic profiles, inflammation, and oxidative stress in impaired glucose tolerance. (2024). https://pubmed.ncbi.nlm.nih.gov/38228168/ DOI: 10.1177/14791641241228156
Complete structured claim and evidence
The zinc-magnesium-chromium regimen did not significantly improve measured metabolic-syndrome risk components, including serum glucose, relative to placebo.
Chromium → Serum glucose concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"}
experimental_model
Double-blind randomized placebo-controlled trial; 32 adults
exposure
24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo
limitations
Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with metabolic syndrome
plain_language
Adding three minerals did not consistently improve the metabolic endpoints in this small trial.
primary_references
[chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022
tissue_or_cell_type
Circulating glucose; the paper describes serum glucose rather than a tissue-specific transport endpoint
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 627–638
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial; 32 adults · source_derived_draft · unverified_draft
### chromium-triple-mineral-glycemia-null The zinc-magnesium-chromium regimen did not significantly improve measured metabolic-syndrome risk components, including serum glucose, relative to placebo. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding three minerals did not consistently improve the metabolic endpoints in this small trial. organism: Human with metabolic syndrome tissue_or_cell_type: Circulating glucose; the paper describes serum glucose rather than a tissue-specific transport endpoint experimental_model: Double-blind randomized placebo-controlled trial; 32 adults limitations: Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints. exposure: 24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo evidence_span: {"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"} [chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022
Complete structured claim and evidence
The three-mineral regimen reduced serum CRP relative to placebo despite the lack of improvement in the measured metabolic-risk components.
Chromium → Serum C-reactive protein concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"}
experimental_model
Double-blind randomized placebo-controlled trial; 32 adults
exposure
24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo
limitations
Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with metabolic syndrome
plain_language
An inflammation marker changed even though the main metabolic measures did not.
primary_references
[chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022
tissue_or_cell_type
Metabolic-risk endpoints and CRP
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 640–651
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial; 32 adults · source_derived_draft · unverified_draft
### chromium-triple-mineral-crp The three-mineral regimen reduced serum CRP relative to placebo despite the lack of improvement in the measured metabolic-risk components. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammation marker changed even though the main metabolic measures did not. organism: Human with metabolic syndrome tissue_or_cell_type: Metabolic-risk endpoints and CRP experimental_model: Double-blind randomized placebo-controlled trial; 32 adults limitations: Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints. exposure: 24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo evidence_span: {"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"} [chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022
Complete structured claim and evidence
HOMA-IR rose in the placebo and vitamin-D3-only groups but was controlled in the chromium and chromium-plus-vitamin-D3 groups.
Chromium(III) picolinate / CrPic → HOMA-IR estimate of insulin resistance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"}
experimental_model
Four-arm randomized supplementation trial; 92 participants
exposure
Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo
limitations
Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes
plain_language
The chromium-containing groups avoided the increase seen in other arms of this trial.
primary_references
[chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
tissue_or_cell_type
Blood glycemia, HOMA-IR and TNF-alpha
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 653–664
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation trial; 92 participants · source_derived_draft · unverified_draft
### chromium-vitd-homa HOMA-IR rose in the placebo and vitamin-D3-only groups but was controlled in the chromium and chromium-plus-vitamin-D3 groups. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chromium-containing groups avoided the increase seen in other arms of this trial. organism: Human with type 2 diabetes tissue_or_cell_type: Blood glycemia, HOMA-IR and TNF-alpha experimental_model: Four-arm randomized supplementation trial; 92 participants limitations: Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested. exposure: Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo evidence_span: {"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"} [chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
Complete structured claim and evidence
TNF-alpha decreased in the vitamin-D3, chromium and combined-treatment groups.
Chromium(III) picolinate / CrPic → Circulating tumor necrosis factor alpha concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"}
experimental_model
Four-arm randomized supplementation trial; 92 participants
exposure
Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo
limitations
Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes
plain_language
The inflammatory marker changed in several active-treatment groups; this does not establish why HOMA-IR differed.
primary_references
[chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
tissue_or_cell_type
Blood glycemia, HOMA-IR and TNF-alpha
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 666–677
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation trial; 92 participants · source_derived_draft · unverified_draft
### chromium-vitd-tnf TNF-alpha decreased in the vitamin-D3, chromium and combined-treatment groups. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inflammatory marker changed in several active-treatment groups; this does not establish why HOMA-IR differed. organism: Human with type 2 diabetes tissue_or_cell_type: Blood glycemia, HOMA-IR and TNF-alpha experimental_model: Four-arm randomized supplementation trial; 92 participants limitations: Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested. exposure: Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo evidence_span: {"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"} [chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
Complete structured claim and evidence
HbA1c, fasting glucose and the lipid profile did not change significantly across the study’s groups.
Chromium(III) picolinate / CrPic → Glycated hemoglobin / HbA1c concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"}
experimental_model
Four-arm randomized supplementation trial; 92 participants
exposure
Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo
limitations
Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes
plain_language
The reported HOMA-IR pattern did not translate into a demonstrated HbA1c improvement.
primary_references
[chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
tissue_or_cell_type
Blood glycemia, HOMA-IR and TNF-alpha
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 679–690
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-arm randomized supplementation trial; 92 participants · source_derived_draft · unverified_draft
### chromium-vitd-hba1c-null HbA1c, fasting glucose and the lipid profile did not change significantly across the study’s groups. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reported HOMA-IR pattern did not translate into a demonstrated HbA1c improvement. organism: Human with type 2 diabetes tissue_or_cell_type: Blood glycemia, HOMA-IR and TNF-alpha experimental_model: Four-arm randomized supplementation trial; 92 participants limitations: Study regimens are historical exposures, not recommendations. Stable versus rising HOMA-IR does not show direct mediation by TNF-alpha; no molecular target was tested. exposure: Four months; vitamin D3 50,000 IU/week, chromium picolinate reported as 500 µg/day, both or placebo evidence_span: {"source_cache": "artifacts/chromium-research/31593637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9", "start_char": 0, "end_char": 1523, "text_sha256": "9815b482cfc5655a11a3192ca21b47c903e8722a3b9b9e7d770e92e9fb94bfa9"} [chromium-p31593637] The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31593637/ DOI: 10.1139/apnm-2019-0113
Complete structured claim and evidence
Fasting glucose changed by −9.8 mg/dL with chromium picolinate plus biotin versus +0.7 mg/dL with placebo (p=0.02).
Chromium(III) picolinate / CrPic → Fasting plasma glucose source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"}
experimental_model
Randomized double-blind placebo-controlled combination trial; 447 enrolled
exposure
600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication
limitations
There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with poorly controlled type 2 diabetes
plain_language
The combination also improved fasting glucose in this trial.
primary_references
[chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755
tissue_or_cell_type
HbA1c and fasting glucose
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 705–716
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled combination trial; 447 enrolled · source_derived_draft · unverified_draft
### chromium-biotin-combination-glucose Fasting glucose changed by −9.8 mg/dL with chromium picolinate plus biotin versus +0.7 mg/dL with placebo (p=0.02). Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination also improved fasting glucose in this trial. organism: Human with poorly controlled type 2 diabetes tissue_or_cell_type: HbA1c and fasting glucose experimental_model: Randomized double-blind placebo-controlled combination trial; 447 enrolled limitations: There were no chromium-only or biotin-only arms. The design cannot identify the active ingredient or prove synergy. Baseline-HbA1c subgroup effects are separately limited. exposure: 600 µg Cr(III) as picolinate plus 2 mg biotin/day for 90 days with stable oral diabetes medication evidence_span: {"source_cache": "artifacts/chromium-research/17506119.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126", "start_char": 0, "end_char": 1739, "text_sha256": "6e79defd1a4209f869bce07c110f0007d02eda63387c2eadc5e014a04c3fc126"} [chromium-p17506119] Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. (2008). https://pubmed.ncbi.nlm.nih.gov/17506119/ DOI: 10.1002/dmrr.755
Complete structured claim and evidence
The chromium-histidinate-plus-biotin condition gave the highest reported GLUT1 protein levels among the compared high-fat-diet interventions in brain and liver.
Chromium(III) histidinate / CrHis → Rat glucose transporter 1 / Slc2a1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}
experimental_model
Six-group high-fat-diet supplementation experiment
exposure
42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure
limitations
No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Sprague-Dawley rats
plain_language
This combination changed GLUT1 abundance in the rat experiment; the independent contribution of chromium was not isolated.
primary_references
[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
tissue_or_cell_type
Brain, liver and systemic metabolism
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 718–729
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft
### chromium-biotin-rat-glut1 The chromium-histidinate-plus-biotin condition gave the highest reported GLUT1 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed GLUT1 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
Complete structured claim and evidence
The chromium-histidinate-plus-biotin condition gave the highest reported GLUT3 protein levels among the compared high-fat-diet interventions in brain and liver.
Chromium(III) histidinate / CrHis → Rat glucose transporter 3 / Slc2a3 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}
experimental_model
Six-group high-fat-diet supplementation experiment
exposure
42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure
limitations
No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Sprague-Dawley rats
plain_language
This combination changed GLUT3 abundance in the rat experiment; the independent contribution of chromium was not isolated.
primary_references
[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
tissue_or_cell_type
Brain, liver and systemic metabolism
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 731–742
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft
### chromium-biotin-rat-glut3 The chromium-histidinate-plus-biotin condition gave the highest reported GLUT3 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed GLUT3 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
Complete structured claim and evidence
The chromium-histidinate-plus-biotin condition gave the highest reported IRS-1 protein levels among the compared high-fat-diet interventions in brain and liver.
Chromium(III) histidinate / CrHis → Rat insulin receptor substrate 1 / Irs1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}
experimental_model
Six-group high-fat-diet supplementation experiment
exposure
42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure
limitations
No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Sprague-Dawley rats
plain_language
This combination changed IRS-1 abundance in the rat experiment; the independent contribution of chromium was not isolated.
primary_references
[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
tissue_or_cell_type
Brain, liver and systemic metabolism
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 744–755
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft
### chromium-biotin-rat-irs1 The chromium-histidinate-plus-biotin condition gave the highest reported IRS-1 protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed IRS-1 abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
Complete structured claim and evidence
The chromium-histidinate-plus-biotin condition gave the highest reported PPAR-gamma protein levels among the compared high-fat-diet interventions in brain and liver.
Chromium(III) histidinate / CrHis → Rat peroxisome proliferator-activated receptor gamma / Pparg source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"}
experimental_model
Six-group high-fat-diet supplementation experiment
exposure
42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure
limitations
No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Sprague-Dawley rats
plain_language
This combination changed PPAR-gamma abundance in the rat experiment; the independent contribution of chromium was not isolated.
primary_references
[chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
tissue_or_cell_type
Brain, liver and systemic metabolism
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 757–768
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-group high-fat-diet supplementation experiment · source_derived_draft · unverified_draft
### chromium-biotin-rat-pparg The chromium-histidinate-plus-biotin condition gave the highest reported PPAR-gamma protein levels among the compared high-fat-diet interventions in brain and liver. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This combination changed PPAR-gamma abundance in the rat experiment; the independent contribution of chromium was not isolated. organism: Male Sprague-Dawley rats tissue_or_cell_type: Brain, liver and systemic metabolism experimental_model: Six-group high-fat-diet supplementation experiment limitations: No chromium-only group in this design. Protein abundance is not proof of a direct target or human cognitive benefit. Product supplied by Nutrition 21; compound-specific comparisons remain scoped. exposure: 42 rats; biotin alone or with chromium histidinate, picolinate or both; 12-week exposure evidence_span: {"source_cache": "artifacts/chromium-research/30680172.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2", "start_char": 0, "end_char": 1282, "text_sha256": "71e98d2ad542eca99d6726b7fb592f311b609e32c0b071375979fb1b79b632c2"} [chromium-p30680172] Effect of supplementing chromium histidinate and picolinate complexes along with biotin on insulin sensitivity and related metabolic indices in rats fed a high-fat diet. (2019). https://pubmed.ncbi.nlm.nih.gov/30680172/ DOI: 10.1002/fsn3.851
Complete structured claim and evidence
Chromium picolinate plus ferric ammonium citrate produced greater insulin-stimulated glucose uptake than ferric ammonium citrate alone in C2C12 cells.
Chromium(III) picolinate / CrPic → Insulin-stimulated glucose uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"}
experimental_model
C2C12 cell experiments with supporting database pathway analysis
exposure
Chromium picolinate, ferric ammonium citrate and combination
limitations
Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse C2C12 skeletal-muscle cells
plain_language
The chromium compound partly countered an iron-induced glucose-uptake defect in cultured cells.
primary_references
[chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
tissue_or_cell_type
Cellular glucose uptake, ROS assays and signaling proteins
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 770–781
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C2C12 cell experiments with supporting database pathway analysis · source_derived_draft · unverified_draft
### chromium-iron-cell-glucose Chromium picolinate plus ferric ammonium citrate produced greater insulin-stimulated glucose uptake than ferric ammonium citrate alone in C2C12 cells. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chromium compound partly countered an iron-induced glucose-uptake defect in cultured cells. organism: Mouse C2C12 skeletal-muscle cells tissue_or_cell_type: Cellular glucose uptake, ROS assays and signaling proteins experimental_model: C2C12 cell experiments with supporting database pathway analysis limitations: Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested. exposure: Chromium picolinate, ferric ammonium citrate and combination evidence_span: {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"} [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
Complete structured claim and evidence
The combination had a lower intracellular ROS assay signal than ferric ammonium citrate alone.
Chromium(III) picolinate / CrPic → Cellular ROS assay signal source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"}
experimental_model
C2C12 cell experiments with supporting database pathway analysis
exposure
Chromium picolinate, ferric ammonium citrate and combination
limitations
Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse C2C12 skeletal-muscle cells
plain_language
A measured oxidative-stress signal was lower with co-treatment.
primary_references
[chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
tissue_or_cell_type
Cellular glucose uptake, ROS assays and signaling proteins
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 783–794
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C2C12 cell experiments with supporting database pathway analysis · source_derived_draft · unverified_draft
### chromium-iron-cell-ros The combination had a lower intracellular ROS assay signal than ferric ammonium citrate alone. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A measured oxidative-stress signal was lower with co-treatment. organism: Mouse C2C12 skeletal-muscle cells tissue_or_cell_type: Cellular glucose uptake, ROS assays and signaling proteins experimental_model: C2C12 cell experiments with supporting database pathway analysis limitations: Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested. exposure: Chromium picolinate, ferric ammonium citrate and combination evidence_span: {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"} [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
Complete structured claim and evidence
Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios.
Chromium(III) picolinate / CrPic → Mouse glucose transporter 4 / Slc2a4 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"}
experimental_model
C2C12 cell experiments with supporting database pathway analysis
exposure
Chromium picolinate, ferric ammonium citrate and combination
limitations
Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Mouse C2C12 skeletal-muscle cells
plain_language
The glucose transporter and measured signaling steps were less suppressed.
primary_references
[chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
tissue_or_cell_type
Cellular glucose uptake, ROS assays and signaling proteins
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 796–807
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C2C12 cell experiments with supporting database pathway analysis · source_derived_draft · unverified_draft
### chromium-iron-cell-glut4 Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose transporter and measured signaling steps were less suppressed. organism: Mouse C2C12 skeletal-muscle cells tissue_or_cell_type: Cellular glucose uptake, ROS assays and signaling proteins experimental_model: C2C12 cell experiments with supporting database pathway analysis limitations: Pathway databases generate hypotheses. Co-changing ROS and signaling measurements do not alone establish a unique causal sequence; no human iron-overload treatment was tested. exposure: Chromium picolinate, ferric ammonium citrate and combination evidence_span: {"source_cache": "artifacts/chromium-research/37156991.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda", "start_char": 0, "end_char": 1621, "text_sha256": "e5b7952975edd461bc01f9a4389588789a7d1b7dedf56fb97270051092ae6cda"} [chromium-p37156991] Antagonizing Effects of Chromium Against Iron-Decreased Glucose Uptake by Regulating ROS-Mediated PI3K/Akt/GLUT4 Signaling Pathway in C2C12. (2024). https://pubmed.ncbi.nlm.nih.gov/37156991/ DOI: 10.1007/s12011-023-03695-z
Complete structured claim and evidence
Chromium picolinate attenuated the pancreatic beta-cell apoptosis associated with iron excess in the rat experiment.
Chromium(III) picolinate / CrPic → Pancreatic beta-cell apoptosis source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"}
experimental_model
Five-group iron-excess supplementation experiment; 30 rats
exposure
Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels
limitations
Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Wistar rats
plain_language
The iron-challenged rats showed less pancreatic-cell injury with chromium treatment.
primary_references
[chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
tissue_or_cell_type
Pancreatic tissue and systemic glucose measures
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 809–820
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-group iron-excess supplementation experiment; 30 rats · source_derived_draft · unverified_draft
### chromium-iron-rat-beta-cell-apoptosis Chromium picolinate attenuated the pancreatic beta-cell apoptosis associated with iron excess in the rat experiment. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The iron-challenged rats showed less pancreatic-cell injury with chromium treatment. organism: Male Wistar rats tissue_or_cell_type: Pancreatic tissue and systemic glucose measures experimental_model: Five-group iron-excess supplementation experiment; 30 rats limitations: Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim. exposure: Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels evidence_span: {"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"} [chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
Complete structured claim and evidence
Chromium treatment countered the iron-associated reduction in pancreatic Bcl-2.
Chromium(III) picolinate / CrPic → Rat Bcl-2 / Bcl2 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"}
experimental_model
Five-group iron-excess supplementation experiment; 30 rats
exposure
Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels
limitations
Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Wistar rats
plain_language
A protein associated with cell survival was better preserved.
primary_references
[chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
tissue_or_cell_type
Pancreatic tissue and systemic glucose measures
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 822–833
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-group iron-excess supplementation experiment; 30 rats · source_derived_draft · unverified_draft
### chromium-iron-rat-bcl2 Chromium treatment countered the iron-associated reduction in pancreatic Bcl-2. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A protein associated with cell survival was better preserved. organism: Male Wistar rats tissue_or_cell_type: Pancreatic tissue and systemic glucose measures experimental_model: Five-group iron-excess supplementation experiment; 30 rats limitations: Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim. exposure: Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels evidence_span: {"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"} [chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
Complete structured claim and evidence
Chromium treatment countered the iron-associated increase in pancreatic Bax.
Chromium(III) picolinate / CrPic → Rat Bax source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"}
experimental_model
Five-group iron-excess supplementation experiment; 30 rats
exposure
Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels
limitations
Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Wistar rats
plain_language
A measured component of the cell-death response was lower.
primary_references
[chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
tissue_or_cell_type
Pancreatic tissue and systemic glucose measures
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 835–846
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-group iron-excess supplementation experiment; 30 rats · source_derived_draft · unverified_draft
### chromium-iron-rat-bax Chromium treatment countered the iron-associated increase in pancreatic Bax. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A measured component of the cell-death response was lower. organism: Male Wistar rats tissue_or_cell_type: Pancreatic tissue and systemic glucose measures experimental_model: Five-group iron-excess supplementation experiment; 30 rats limitations: Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim. exposure: Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels evidence_span: {"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"} [chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
Complete structured claim and evidence
Chromium treatment countered the iron-associated increase in pancreatic cleaved caspase-9.
Chromium(III) picolinate / CrPic → Rat cleaved caspase-9 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"}
experimental_model
Five-group iron-excess supplementation experiment; 30 rats
exposure
Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels
limitations
Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Wistar rats
plain_language
A later component of the cell-death pathway was lower.
primary_references
[chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
tissue_or_cell_type
Pancreatic tissue and systemic glucose measures
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 848–859
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-group iron-excess supplementation experiment; 30 rats · source_derived_draft · unverified_draft
### chromium-iron-rat-caspase9 Chromium treatment countered the iron-associated increase in pancreatic cleaved caspase-9. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A later component of the cell-death pathway was lower. organism: Male Wistar rats tissue_or_cell_type: Pancreatic tissue and systemic glucose measures experimental_model: Five-group iron-excess supplementation experiment; 30 rats limitations: Small animal experiment with multiple measured changes. Pathway mediation was proposed, not established by a complete intervention on each signaling node; no human treatment or dietary rescue claim. exposure: Eight weeks; adequate or excessive iron as iron citrate with three chromium-picolinate dose levels evidence_span: {"source_cache": "artifacts/chromium-research/41108476.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3", "start_char": 0, "end_char": 1865, "text_sha256": "7c71767b7a3b58e61b7961f55febf9d637807fe598539f4257a3b1e40fe03fb3"} [chromium-p41108476] Chromium Mitigates the Iron-Induced Glucose Metabolism Disorder via the PI3K/Akt/Bcl-2 Signaling Pathway: An In Vivo Study in Wistar Rats. (2026). https://pubmed.ncbi.nlm.nih.gov/41108476/ DOI: 10.1007/s12011-025-04867-9
Complete structured claim and evidence
Oral coadministration of nicotinic acid with labeled chromium did not significantly alter chromium retention in the rat study.
Nicotinic acid → Whole-body chromium retention source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/8605085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889", "start_char": 0, "end_char": 1103, "text_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889"}
experimental_model
Oral radiotracer retention and distribution experiments
exposure
Labeled oral chromium with dietary/metabolite coadministration
limitations
A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat
plain_language
Adding nicotinic acid did not make the rats retain more chromium in this experiment.
primary_references
[chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412
tissue_or_cell_type
Whole-body and tissue chromium
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 861–872
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral radiotracer retention and distribution experiments · source_derived_draft · unverified_draft
### chromium-niacin-retention-null Oral coadministration of nicotinic acid with labeled chromium did not significantly alter chromium retention in the rat study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding nicotinic acid did not make the rats retain more chromium in this experiment. organism: Rat tissue_or_cell_type: Whole-body and tissue chromium experimental_model: Oral radiotracer retention and distribution experiments limitations: A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex. exposure: Labeled oral chromium with dietary/metabolite coadministration evidence_span: {"source_cache": "artifacts/chromium-research/8605085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889", "start_char": 0, "end_char": 1103, "text_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889"} [chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412
Complete structured claim and evidence
Oral coadministration of glutathione with labeled chromium did not significantly alter chromium retention in the rat study.
GSH → Whole-body chromium retention source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/8605085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889", "start_char": 0, "end_char": 1103, "text_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889"}
experimental_model
Oral radiotracer retention and distribution experiments
exposure
Labeled oral chromium with dietary/metabolite coadministration
limitations
A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Rat
plain_language
Adding glutathione did not make the rats retain more chromium in this experiment.
primary_references
[chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412
tissue_or_cell_type
Whole-body and tissue chromium
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 874–885
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral radiotracer retention and distribution experiments · source_derived_draft · unverified_draft
### chromium-gsh-retention-null Oral coadministration of glutathione with labeled chromium did not significantly alter chromium retention in the rat study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding glutathione did not make the rats retain more chromium in this experiment. organism: Rat tissue_or_cell_type: Whole-body and tissue chromium experimental_model: Oral radiotracer retention and distribution experiments limitations: A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex. exposure: Labeled oral chromium with dietary/metabolite coadministration evidence_span: {"source_cache": "artifacts/chromium-research/8605085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889", "start_char": 0, "end_char": 1103, "text_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889"} [chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412
Complete structured claim and evidence
Peripheral nerve conduction returned to normal over the subsequent five-month period in the 1977 parenteral-nutrition case.
Chromium → Peripheral nerve conduction source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/192066.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c", "start_char": 0, "end_char": 1943, "text_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c"}
experimental_model
Historical long-term parenteral-nutrition case report
exposure
More than five years of parenteral nutrition; 250 µg chromium/day added for two weeks after impaired glucose tolerance and neuropathy
limitations
Single uncontrolled case with complex nutrition and treatment changes. Historical blood/hair reference ranges are not validated current diagnostic thresholds; response to pharmacological chromium does not by itself prove an essential dietary requirement.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human adult patient
plain_language
The neurological measurements also improved during follow-up.
primary_references
[chromium-p192066] Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation, in a patient receiving long-term total parenteral nutrition. (1977). https://pubmed.ncbi.nlm.nih.gov/192066/ DOI: 10.1093/ajcn/30.4.531
tissue_or_cell_type
Systemic glucose utilization and peripheral nerves
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 900–911
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical long-term parenteral-nutrition case report · source_derived_draft · unverified_draft
### chromium-parenteral-neuropathy-1977 Peripheral nerve conduction returned to normal over the subsequent five-month period in the 1977 parenteral-nutrition case. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The neurological measurements also improved during follow-up. organism: Human adult patient tissue_or_cell_type: Systemic glucose utilization and peripheral nerves experimental_model: Historical long-term parenteral-nutrition case report limitations: Single uncontrolled case with complex nutrition and treatment changes. Historical blood/hair reference ranges are not validated current diagnostic thresholds; response to pharmacological chromium does not by itself prove an essential dietary requirement. exposure: More than five years of parenteral nutrition; 250 µg chromium/day added for two weeks after impaired glucose tolerance and neuropathy evidence_span: {"source_cache": "artifacts/chromium-research/192066.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c", "start_char": 0, "end_char": 1943, "text_sha256": "77f1130259582a7565cecbf7bf6d04dd0f54fb6c54ebf8d4498341c48ec3cd8c"} [chromium-p192066] Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation, in a patient receiving long-term total parenteral nutrition. (1977). https://pubmed.ncbi.nlm.nih.gov/192066/ DOI: 10.1093/ajcn/30.4.531
Complete structured claim and evidence
Chromium addition was followed by improved glucose tolerance, reduced insulin requirements, weight gain and disappearance of a confusional state in the 1979 case.
Chromium → Glucose tolerance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/104057.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "858c83b6633bd3a8c4efd76fa98e12e487db932eda817827319066281fbcd6da", "start_char": 0, "end_char": 655, "text_sha256": "858c83b6633bd3a8c4efd76fa98e12e487db932eda817827319066281fbcd6da"}
experimental_model
Historical post-bowel-resection parenteral-nutrition case report
exposure
Five months parenteral nutrition; 150 µg chromium/day supplementation
limitations
Uncontrolled case, with serum chromium described as at the low end of the then-normal range. No validated modern deficiency threshold or molecular mediator established.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human patient
plain_language
A second historical case reported improvement, while the cause and broader applicability remain uncertain.
primary_references
[chromium-p104057] Chromium deficiency during total parenteral nutrition. (1979). https://pubmed.ncbi.nlm.nih.gov/104057/ DOI: 10.1001/jama.1979.03290310036012
tissue_or_cell_type
Glucose regulation, weight and neurological state
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 913–924
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical post-bowel-resection parenteral-nutrition case report · source_derived_draft · unverified_draft
### chromium-parenteral-glucose-1979 Chromium addition was followed by improved glucose tolerance, reduced insulin requirements, weight gain and disappearance of a confusional state in the 1979 case. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second historical case reported improvement, while the cause and broader applicability remain uncertain. organism: Human patient tissue_or_cell_type: Glucose regulation, weight and neurological state experimental_model: Historical post-bowel-resection parenteral-nutrition case report limitations: Uncontrolled case, with serum chromium described as at the low end of the then-normal range. No validated modern deficiency threshold or molecular mediator established. exposure: Five months parenteral nutrition; 150 µg chromium/day supplementation evidence_span: {"source_cache": "artifacts/chromium-research/104057.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "858c83b6633bd3a8c4efd76fa98e12e487db932eda817827319066281fbcd6da", "start_char": 0, "end_char": 655, "text_sha256": "858c83b6633bd3a8c4efd76fa98e12e487db932eda817827319066281fbcd6da"} [chromium-p104057] Chromium deficiency during total parenteral nutrition. (1979). https://pubmed.ncbi.nlm.nih.gov/104057/ DOI: 10.1001/jama.1979.03290310036012
Complete structured claim and evidence
Plasma chromium increased with longer parenteral-nutrition exposure even when the trace-mineral supplement contained no chromium.
Chromium → Circulating chromium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/39898458.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7", "start_char": 0, "end_char": 1530, "text_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7"}
experimental_model
Prospective observational study; 97 very-low-birthweight infants
exposure
Parenteral nutrition without added chromium from day 1; plasma days 15/30 and urine day 30
limitations
No added chromium does not mean zero exposure because components can contain chromium. Observational biomarker findings do not establish adequacy thresholds or universal neonatal dosing guidance.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human premature infants
plain_language
The infants were still exposed to chromium through the nutrition system.
primary_references
[chromium-p39898458] Chromium-free parenteral nutrition and its effects on chromium levels in very low birth weight infants. (2025). https://pubmed.ncbi.nlm.nih.gov/39898458/ DOI: 10.20960/nh.05609
tissue_or_cell_type
Plasma and urine during neonatal nutrition
trigger_kind
biomarker_context Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 926–937
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective observational study; 97 very-low-birthweight infants · source_derived_draft · unverified_draft
### chromium-neonatal-pn-exposure Plasma chromium increased with longer parenteral-nutrition exposure even when the trace-mineral supplement contained no chromium. Condition category: biomarker_context nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The infants were still exposed to chromium through the nutrition system. organism: Human premature infants tissue_or_cell_type: Plasma and urine during neonatal nutrition experimental_model: Prospective observational study; 97 very-low-birthweight infants limitations: No added chromium does not mean zero exposure because components can contain chromium. Observational biomarker findings do not establish adequacy thresholds or universal neonatal dosing guidance. exposure: Parenteral nutrition without added chromium from day 1; plasma days 15/30 and urine day 30 evidence_span: {"source_cache": "artifacts/chromium-research/39898458.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7", "start_char": 0, "end_char": 1530, "text_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7"} [chromium-p39898458] Chromium-free parenteral nutrition and its effects on chromium levels in very low birth weight infants. (2025). https://pubmed.ncbi.nlm.nih.gov/39898458/ DOI: 10.20960/nh.05609
Complete structured claim and evidence
The neonatal study found no relation of measured plasma or urinary chromium to its assessed laboratory parameters or morbidity.
Circulating chromium concentration → Neonatal morbidity measurements source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/39898458.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7", "start_char": 0, "end_char": 1530, "text_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7"}
experimental_model
Prospective observational study; 97 very-low-birthweight infants
exposure
Parenteral nutrition without added chromium from day 1; plasma days 15/30 and urine day 30
limitations
No added chromium does not mean zero exposure because components can contain chromium. Observational biomarker findings do not establish adequacy thresholds or universal neonatal dosing guidance.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human premature infants
plain_language
The measured chromium differences were not linked to the reported clinical outcomes.
primary_references
[chromium-p39898458] Chromium-free parenteral nutrition and its effects on chromium levels in very low birth weight infants. (2025). https://pubmed.ncbi.nlm.nih.gov/39898458/ DOI: 10.20960/nh.05609
tissue_or_cell_type
Plasma and urine during neonatal nutrition
trigger_kind
biomarker_context Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 939–950
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective observational study; 97 very-low-birthweight infants · source_derived_draft · unverified_draft
### chromium-neonatal-marker-outcome-null The neonatal study found no relation of measured plasma or urinary chromium to its assessed laboratory parameters or morbidity. Condition category: biomarker_context nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured chromium differences were not linked to the reported clinical outcomes. organism: Human premature infants tissue_or_cell_type: Plasma and urine during neonatal nutrition experimental_model: Prospective observational study; 97 very-low-birthweight infants limitations: No added chromium does not mean zero exposure because components can contain chromium. Observational biomarker findings do not establish adequacy thresholds or universal neonatal dosing guidance. exposure: Parenteral nutrition without added chromium from day 1; plasma days 15/30 and urine day 30 evidence_span: {"source_cache": "artifacts/chromium-research/39898458.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7", "start_char": 0, "end_char": 1530, "text_sha256": "1776af33c0e684df33140b02e64d6cb2b4fa727cc167e6b17662e0f4c74275c7"} [chromium-p39898458] Chromium-free parenteral nutrition and its effects on chromium levels in very low birth weight infants. (2025). https://pubmed.ncbi.nlm.nih.gov/39898458/ DOI: 10.20960/nh.05609
Complete structured claim and evidence
Supplemented diets produced lower insulin-response areas after glucose challenge than the low-chromium diet, despite the lack of a glucose-tolerance defect.
Chromium → Plasma insulin response to glucose challenge source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/21086001.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd", "start_char": 0, "end_char": 1561, "text_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd"}
experimental_model
Six-month metal-controlled low-chromium feeding experiment
exposure
AIN-93G with no added chromium versus standard diet and supplemental 200 or 1,000 µg Cr/kg
limitations
Low intake is not absolute zero exposure. Lack of abnormality in this rat model challenges essentiality claims but is not by itself a complete human requirement experiment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Male Zucker lean rats
plain_language
A pharmacological response can occur even when the low-intake group has no demonstrated deficiency syndrome.
primary_references
[chromium-p21086001] Chromium is not an essential trace element for mammals: effects of a "low-chromium" diet. (2011). https://pubmed.ncbi.nlm.nih.gov/21086001/ DOI: 10.1007/s00775-010-0734-y
tissue_or_cell_type
Body composition and glucose/insulin tolerance
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 965–976
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month metal-controlled low-chromium feeding experiment · source_derived_draft · unverified_draft
### chromium-supplement-insulin-auc-2011 Supplemented diets produced lower insulin-response areas after glucose challenge than the low-chromium diet, despite the lack of a glucose-tolerance defect. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pharmacological response can occur even when the low-intake group has no demonstrated deficiency syndrome. organism: Male Zucker lean rats tissue_or_cell_type: Body composition and glucose/insulin tolerance experimental_model: Six-month metal-controlled low-chromium feeding experiment limitations: Low intake is not absolute zero exposure. Lack of abnormality in this rat model challenges essentiality claims but is not by itself a complete human requirement experiment. exposure: AIN-93G with no added chromium versus standard diet and supplemental 200 or 1,000 µg Cr/kg evidence_span: {"source_cache": "artifacts/chromium-research/21086001.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd", "start_char": 0, "end_char": 1561, "text_sha256": "308018cb4483d2b09c61c09f63a45811cc801750fd4f7922b8c9f010f5165abd"} [chromium-p21086001] Chromium is not an essential trace element for mammals: effects of a "low-chromium" diet. (2011). https://pubmed.ncbi.nlm.nih.gov/21086001/ DOI: 10.1007/s00775-010-0734-y
Complete structured claim and evidence
The low-chromium group had higher fasting insulin and higher insulin at 30 and 60 minutes after glucose than the normal-chromium group, without a difference in glucose levels.
Chromium → Fasting plasma insulin concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"}
experimental_model
Twelve-week dietary chromium experiment in both sexes
exposure
From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group
limitations
Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Sprague-Dawley CD rats
plain_language
The animals needed a different insulin response while measured glucose stayed similar.
primary_references
[chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
tissue_or_cell_type
Whole-body fat and circulating metabolic measures
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 978–989
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve-week dietary chromium experiment in both sexes · source_derived_draft · unverified_draft
### chromium-low-diet-insulin-2023 The low-chromium group had higher fasting insulin and higher insulin at 30 and 60 minutes after glucose than the normal-chromium group, without a difference in glucose levels. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The animals needed a different insulin response while measured glucose stayed similar. organism: Sprague-Dawley CD rats tissue_or_cell_type: Whole-body fat and circulating metabolic measures experimental_model: Twelve-week dietary chromium experiment in both sexes limitations: Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff. exposure: From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group evidence_span: {"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"} [chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
Complete structured claim and evidence
The low-chromium group consumed more energy later in the experiment and accumulated more body fat than the normal-chromium group.
Chromium → Whole-body fat mass source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"}
experimental_model
Twelve-week dietary chromium experiment in both sexes
exposure
From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group
limitations
Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Sprague-Dawley CD rats
plain_language
The result involved food intake and body composition as well as glucose-related measurements.
primary_references
[chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
tissue_or_cell_type
Whole-body fat and circulating metabolic measures
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 991–1002
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve-week dietary chromium experiment in both sexes · source_derived_draft · unverified_draft
### chromium-low-diet-fat-2023 The low-chromium group consumed more energy later in the experiment and accumulated more body fat than the normal-chromium group. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The result involved food intake and body composition as well as glucose-related measurements. organism: Sprague-Dawley CD rats tissue_or_cell_type: Whole-body fat and circulating metabolic measures experimental_model: Twelve-week dietary chromium experiment in both sexes limitations: Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff. exposure: From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group evidence_span: {"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"} [chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
Complete structured claim and evidence
Fasting triglycerides were higher in the low-chromium group than the normal-chromium group at the end of the rat experiment.
Chromium → Plasma triglyceride concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"}
experimental_model
Twelve-week dietary chromium experiment in both sexes
exposure
From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group
limitations
Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Sprague-Dawley CD rats
plain_language
The lower-chromium diet also changed a circulating lipid measurement.
primary_references
[chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
tissue_or_cell_type
Whole-body fat and circulating metabolic measures
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1004–1015
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve-week dietary chromium experiment in both sexes · source_derived_draft · unverified_draft
### chromium-low-diet-triglycerides-2023 Fasting triglycerides were higher in the low-chromium group than the normal-chromium group at the end of the rat experiment. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The lower-chromium diet also changed a circulating lipid measurement. organism: Sprague-Dawley CD rats tissue_or_cell_type: Whole-body fat and circulating metabolic measures experimental_model: Twelve-week dietary chromium experiment in both sexes limitations: Different diet, strain and duration from the 2011 study. Greater food intake can contribute to adiposity and insulin changes. Low is relative to this rodent formulation, not a human deficiency cutoff. exposure: From day 35 of age; moderately high-fat/high-sucrose diets with 0.33, 1.20 or 9.15 mg Cr/kg; 10 males and 10 females/group evidence_span: {"source_cache": "artifacts/chromium-research/36701335.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48", "start_char": 0, "end_char": 1806, "text_sha256": "762bdd075019b97831308c39060063214abcb5c5075bfc69afd9b1e250b41a48"} [chromium-p36701335] A low chromium diet increases body fat, energy intake and circulating triglycerides and insulin in male and female rats fed a moderately high-fat, high-sucrose diet from peripuberty to young adult age. (2023). https://pubmed.ncbi.nlm.nih.gov/36701335/ DOI: 10.1371/journal.pone.0281019
Complete structured claim and evidence
The 1,000 µg/day group had lower fasting glucose than placebo at two and four months; four-month values were 7.1 versus 8.8 mmol/L.
Chromium(III) picolinate / CrPic → Fasting plasma glucose source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"}
experimental_model
Randomized three-arm supplementation trial; 180 adults
exposure
Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued
limitations
Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with treated type 2 diabetes
plain_language
Fasting glucose was also lower in the higher-dose group.
primary_references
[chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
tissue_or_cell_type
HbA1c, glucose, insulin and lipids
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1030–1041
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-arm supplementation trial; 180 adults · source_derived_draft · unverified_draft
### chromium-diabetes-fasting-glucose-positive The 1,000 µg/day group had lower fasting glucose than placebo at two and four months; four-month values were 7.1 versus 8.8 mmol/L. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fasting glucose was also lower in the higher-dose group. organism: Human with treated type 2 diabetes tissue_or_cell_type: HbA1c, glucose, insulin and lipids experimental_model: Randomized three-arm supplementation trial; 180 adults limitations: Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects. exposure: Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued evidence_span: {"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"} [chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
Complete structured claim and evidence
Fasting and two-hour insulin measurements decreased in both chromium-supplemented groups in the reported study.
Chromium(III) picolinate / CrPic → Fasting plasma insulin concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"}
experimental_model
Randomized three-arm supplementation trial; 180 adults
exposure
Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued
limitations
Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with treated type 2 diabetes
plain_language
The study reported an insulin change alongside its glucose findings.
primary_references
[chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
tissue_or_cell_type
HbA1c, glucose, insulin and lipids
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1043–1054
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-arm supplementation trial; 180 adults · source_derived_draft · unverified_draft
### chromium-diabetes-insulin-positive Fasting and two-hour insulin measurements decreased in both chromium-supplemented groups in the reported study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study reported an insulin change alongside its glucose findings. organism: Human with treated type 2 diabetes tissue_or_cell_type: HbA1c, glucose, insulin and lipids experimental_model: Randomized three-arm supplementation trial; 180 adults limitations: Historical single-population trial; response does not diagnose chromium deficiency. Baseline diet, medication context and replication matter; later trials reported null effects. exposure: Placebo, 200 or 1,000 µg Cr/day as picolinate for four months while usual medications continued evidence_span: {"source_cache": "artifacts/chromium-research/9356027.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69", "start_char": 0, "end_char": 1941, "text_sha256": "9c9f5146517d1c6967a6f75951c79fbb828408e96693be5df98f9fb1ec91aa69"} [chromium-p9356027] Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. (1997). https://pubmed.ncbi.nlm.nih.gov/9356027/ DOI: 10.2337/diab.46.11.1786
Complete structured claim and evidence
The chromium-plus-sulfonylurea group showed improved measured insulin sensitivity and glucose control compared with the study’s sulfonylurea/placebo comparison.
Chromium(III) picolinate / CrPic → Insulin sensitivity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/16873787.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8b9da2c39dd1dde1b2aba2fe7db1f7b9330d110b1594f3ee96df161840f731c", "start_char": 0, "end_char": 1823, "text_sha256": "e8b9da2c39dd1dde1b2aba2fe7db1f7b9330d110b1594f3ee96df161840f731c"}
experimental_model
Double-blind randomized trial after sulfonylurea run-in
exposure
Glipizide run-in then 1,000 µg Cr/day as picolinate or placebo for six months; randomized groups n=17 and n=12
limitations
Small trial with concurrent glipizide. Reported benefit does not establish chromium deficiency, isolate every mediator or generalize to other treatment populations.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes
plain_language
This smaller trial reported benefit in a different medication setting.
primary_references
[chromium-p16873787] Chromium picolinate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes. (2006). https://pubmed.ncbi.nlm.nih.gov/16873787/ DOI: 10.2337/dc06-0254
tissue_or_cell_type
Insulin sensitivity, glycated hemoglobin and body composition
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1069–1080
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized trial after sulfonylurea run-in · source_derived_draft · unverified_draft
### chromium-glipizide-trial-sensitivity The chromium-plus-sulfonylurea group showed improved measured insulin sensitivity and glucose control compared with the study’s sulfonylurea/placebo comparison. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This smaller trial reported benefit in a different medication setting. organism: Human with type 2 diabetes tissue_or_cell_type: Insulin sensitivity, glycated hemoglobin and body composition experimental_model: Double-blind randomized trial after sulfonylurea run-in limitations: Small trial with concurrent glipizide. Reported benefit does not establish chromium deficiency, isolate every mediator or generalize to other treatment populations. exposure: Glipizide run-in then 1,000 µg Cr/day as picolinate or placebo for six months; randomized groups n=17 and n=12 evidence_span: {"source_cache": "artifacts/chromium-research/16873787.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8b9da2c39dd1dde1b2aba2fe7db1f7b9330d110b1594f3ee96df161840f731c", "start_char": 0, "end_char": 1823, "text_sha256": "e8b9da2c39dd1dde1b2aba2fe7db1f7b9330d110b1594f3ee96df161840f731c"} [chromium-p16873787] Chromium picolinate supplementation attenuates body weight gain and increases insulin sensitivity in subjects with type 2 diabetes. (2006). https://pubmed.ncbi.nlm.nih.gov/16873787/ DOI: 10.2337/dc06-0254
Complete structured claim and evidence
Chromium did not consistently improve insulin action across the full phenotype range; response-defined subgroups differed in baseline insulin resistance and glycemia but not chromium status.
Chromium → Insulin sensitivity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/20022616.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2", "start_char": 0, "end_char": 1864, "text_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2"}
experimental_model
Randomized supplementation with euglycemic-clamp and tissue-lipid substudy
exposure
1,000 µg chromium/day or placebo; responders classified by ≥10% change in insulin sensitivity
limitations
Response-defined subgroup comparisons can be affected by regression to the mean and post-treatment selection. They do not validate a deficiency test or a prospective rule for choosing treatment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes across a range of phenotypes
plain_language
Not everyone responded, and the measured chromium level did not distinguish responders from nonresponders.
primary_references
[chromium-p20022616] Characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus. (2010). https://pubmed.ncbi.nlm.nih.gov/20022616/ DOI: 10.1016/j.metabol.2009.09.023
tissue_or_cell_type
Insulin sensitivity, muscle/liver lipid and chromium measurements
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1082–1093
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized supplementation with euglycemic-clamp and tissue-lipid substudy · source_derived_draft · unverified_draft
### chromium-human-response-heterogeneity Chromium did not consistently improve insulin action across the full phenotype range; response-defined subgroups differed in baseline insulin resistance and glycemia but not chromium status. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Not everyone responded, and the measured chromium level did not distinguish responders from nonresponders. organism: Human with type 2 diabetes across a range of phenotypes tissue_or_cell_type: Insulin sensitivity, muscle/liver lipid and chromium measurements experimental_model: Randomized supplementation with euglycemic-clamp and tissue-lipid substudy limitations: Response-defined subgroup comparisons can be affected by regression to the mean and post-treatment selection. They do not validate a deficiency test or a prospective rule for choosing treatment. exposure: 1,000 µg chromium/day or placebo; responders classified by ≥10% change in insulin sensitivity evidence_span: {"source_cache": "artifacts/chromium-research/20022616.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2", "start_char": 0, "end_char": 1864, "text_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2"} [chromium-p20022616] Characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus. (2010). https://pubmed.ncbi.nlm.nih.gov/20022616/ DOI: 10.1016/j.metabol.2009.09.023
Complete structured claim and evidence
Subjects randomized to chromium had lower intramyocellular lipid measurements in the substudy.
Chromium → Intramyocellular lipid content source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/20022616.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2", "start_char": 0, "end_char": 1864, "text_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2"}
experimental_model
Randomized supplementation with euglycemic-clamp and tissue-lipid substudy
exposure
1,000 µg chromium/day or placebo; responders classified by ≥10% change in insulin sensitivity
limitations
Response-defined subgroup comparisons can be affected by regression to the mean and post-treatment selection. They do not validate a deficiency test or a prospective rule for choosing treatment.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human with type 2 diabetes across a range of phenotypes
plain_language
A muscle-lipid measurement changed, offering a possible research lead rather than a proven universal mediator.
primary_references
[chromium-p20022616] Characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus. (2010). https://pubmed.ncbi.nlm.nih.gov/20022616/ DOI: 10.1016/j.metabol.2009.09.023
tissue_or_cell_type
Insulin sensitivity, muscle/liver lipid and chromium measurements
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1095–1106
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized supplementation with euglycemic-clamp and tissue-lipid substudy · source_derived_draft · unverified_draft
### chromium-human-muscle-lipid Subjects randomized to chromium had lower intramyocellular lipid measurements in the substudy. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A muscle-lipid measurement changed, offering a possible research lead rather than a proven universal mediator. organism: Human with type 2 diabetes across a range of phenotypes tissue_or_cell_type: Insulin sensitivity, muscle/liver lipid and chromium measurements experimental_model: Randomized supplementation with euglycemic-clamp and tissue-lipid substudy limitations: Response-defined subgroup comparisons can be affected by regression to the mean and post-treatment selection. They do not validate a deficiency test or a prospective rule for choosing treatment. exposure: 1,000 µg chromium/day or placebo; responders classified by ≥10% change in insulin sensitivity evidence_span: {"source_cache": "artifacts/chromium-research/20022616.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2", "start_char": 0, "end_char": 1864, "text_sha256": "0c9e6d805526dd6fa08c3a57f750df6d1f2312932e04ea8c3ce7975f46d65ab2"} [chromium-p20022616] Characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus. (2010). https://pubmed.ncbi.nlm.nih.gov/20022616/ DOI: 10.1016/j.metabol.2009.09.023
Complete structured claim and evidence
Neither tested dose improved glucose, insulin or HOMA-IR compared with placebo after six months; secondary outcomes also did not improve.
Chromium(III) picolinate / CrPic → HOMA-IR estimate of insulin resistance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/20634174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8a4617886df8215ff55fd78eac2a60d4e63ed726da4f1f1a9167fb9c41ceae26", "start_char": 0, "end_char": 1529, "text_sha256": "8a4617886df8215ff55fd78eac2a60d4e63ed726da4f1f1a9167fb9c41ceae26"}
experimental_model
Randomized double-blind modified crossover trial; 59 enrolled
exposure
Six-month sequences of 500 or 1,000 µg/day chromium picolinate versus placebo
limitations
At-risk population rather than established diabetes; no demonstrated prevention effect. Exposure does not establish the participant’s nutritional chromium status.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human adults at high risk for type 2 diabetes
plain_language
The supplement did not improve the measured insulin-resistance outcomes in this at-risk group.
primary_references
[chromium-p20634174] Chromium effects on glucose tolerance and insulin sensitivity in persons at risk for diabetes mellitus. (2011). https://pubmed.ncbi.nlm.nih.gov/20634174/ DOI: 10.4158/ep10131.or
tissue_or_cell_type
Glucose, insulin, HOMA-IR and secondary cardiometabolic endpoints
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1108–1119
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind modified crossover trial; 59 enrolled · source_derived_draft · unverified_draft
### chromium-prediabetes-null Neither tested dose improved glucose, insulin or HOMA-IR compared with placebo after six months; secondary outcomes also did not improve. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The supplement did not improve the measured insulin-resistance outcomes in this at-risk group. organism: Human adults at high risk for type 2 diabetes tissue_or_cell_type: Glucose, insulin, HOMA-IR and secondary cardiometabolic endpoints experimental_model: Randomized double-blind modified crossover trial; 59 enrolled limitations: At-risk population rather than established diabetes; no demonstrated prevention effect. Exposure does not establish the participant’s nutritional chromium status. exposure: Six-month sequences of 500 or 1,000 µg/day chromium picolinate versus placebo evidence_span: {"source_cache": "artifacts/chromium-research/20634174.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8a4617886df8215ff55fd78eac2a60d4e63ed726da4f1f1a9167fb9c41ceae26", "start_char": 0, "end_char": 1529, "text_sha256": "8a4617886df8215ff55fd78eac2a60d4e63ed726da4f1f1a9167fb9c41ceae26"} [chromium-p20634174] Chromium effects on glucose tolerance and insulin sensitivity in persons at risk for diabetes mellitus. (2011). https://pubmed.ncbi.nlm.nih.gov/20634174/ DOI: 10.4158/ep10131.or
Complete structured claim and evidence
Ascorbate restoration prevented Cr(VI)-induced ATM activation observed in standard ascorbate-poor human lung-cell cultures.
L-Ascorbate → Human ATM kinase source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
experimental_model
Ascorbate restoration and ATM perturbation in human lung-cell cultures
exposure
Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
limitations
Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human H460 cells and normal lung fibroblasts
plain_language
Vitamin C availability changed which damage-response pathway the toxic exposure activated.
primary_references
[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
tissue_or_cell_type
DNA-damage signaling
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1121–1132
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft
### chromium-ascorbate-atm-context Ascorbate restoration prevented Cr(VI)-induced ATM activation observed in standard ascorbate-poor human lung-cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C availability changed which damage-response pathway the toxic exposure activated. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
Complete structured claim and evidence
Chromate exposure induced CHK2 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures.
Chromate / chromium(VI) oxyanion → Human checkpoint kinase 2 / CHEK2 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
experimental_model
Ascorbate restoration and ATM perturbation in human lung-cell cultures
exposure
Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
limitations
Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human H460 cells and normal lung fibroblasts
plain_language
This downstream damage-response protein changed in the low-ascorbate culture condition.
primary_references
[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
tissue_or_cell_type
DNA-damage signaling
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1134–1145
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft
### chromium-chromate-chk2 Chromate exposure induced CHK2 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
Complete structured claim and evidence
Chromate exposure induced KAP1 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures.
Chromate / chromium(VI) oxyanion → Human KAP1 / TRIM28 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}
experimental_model
Ascorbate restoration and ATM perturbation in human lung-cell cultures
exposure
Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing
limitations
Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Human H460 cells and normal lung fibroblasts
plain_language
This downstream damage-response protein changed in the low-ascorbate culture condition.
primary_references
[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
tissue_or_cell_type
DNA-damage signaling
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1147–1158
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft
### chromium-chromate-kap1 Chromate exposure induced KAP1 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434
Complete structured claim and evidence
Chromate reduction with 2 mM glutathione produced weak plasmid mutagenicity; 5 mM glutathione produced about four times the mutation yield per DNA adduct.
GSH → Mutation induction by chromium-treated DNA source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"}
experimental_model
Cell-free chromate reduction followed by plasmid replication in human fibroblasts
exposure
2 versus 5 mM glutathione with Cr(VI)
limitations
Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Chemical system with human fibroblast mutagenicity readout
plain_language
More glutathione did not simply mean less damage in this chemical system.
primary_references
[chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g
tissue_or_cell_type
DNA reaction mixture and reporter plasmid
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1160–1171
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free chromate reduction followed by plasmid replication in human fibroblasts · source_derived_draft · unverified_draft
### chromium-gsh-chromate-mutagenesis Chromate reduction with 2 mM glutathione produced weak plasmid mutagenicity; 5 mM glutathione produced about four times the mutation yield per DNA adduct. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glutathione did not simply mean less damage in this chemical system. organism: Chemical system with human fibroblast mutagenicity readout tissue_or_cell_type: DNA reaction mixture and reporter plasmid experimental_model: Cell-free chromate reduction followed by plasmid replication in human fibroblasts limitations: Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations. exposure: 2 versus 5 mM glutathione with Cr(VI) evidence_span: {"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"} [chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g
Complete structured claim and evidence
The study attributed about 5% of total chromium-DNA adducts to GSH-Cr-DNA crosslinks at 2 mM glutathione, with four- to fivefold higher crosslinking at 5 mM.
GSH → Reported glutathione–chromium–DNA ternary adduct source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"}
experimental_model
Cell-free chromate reduction followed by plasmid replication in human fibroblasts
exposure
2 versus 5 mM glutathione with Cr(VI)
limitations
Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Chemical system with human fibroblast mutagenicity readout
plain_language
The authors detected and assigned a glutathione-linked DNA lesion; the preparation and analytical assignment matter.
primary_references
[chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g
tissue_or_cell_type
DNA reaction mixture and reporter plasmid
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1173–1184
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free chromate reduction followed by plasmid replication in human fibroblasts · source_derived_draft · unverified_draft
### chromium-gsh-chromate-adducts The study attributed about 5% of total chromium-DNA adducts to GSH-Cr-DNA crosslinks at 2 mM glutathione, with four- to fivefold higher crosslinking at 5 mM. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The authors detected and assigned a glutathione-linked DNA lesion; the preparation and analytical assignment matter. organism: Chemical system with human fibroblast mutagenicity readout tissue_or_cell_type: DNA reaction mixture and reporter plasmid experimental_model: Cell-free chromate reduction followed by plasmid replication in human fibroblasts limitations: Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations. exposure: 2 versus 5 mM glutathione with Cr(VI) evidence_span: {"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"} [chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g
Complete structured claim and evidence
The characterized pre-reacted Cr(III)-cysteine, -glutathione and -ascorbate preparations did not measurably bind DNA or form the proposed ternary adducts under the tested conditions.
Trivalent chromium / Cr(III) → Formation of chromium–small-molecule–DNA ternary adducts source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chromium-research/36662348.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "500f334d72ca34561016a11f0c3bf866998ee364085855e54a2f29025bc916a8", "start_char": 0, "end_char": 1155, "text_sha256": "500f334d72ca34561016a11f0c3bf866998ee364085855e54a2f29025bc916a8"}
experimental_model
Characterization of pre-reacted chromium-ligand preparations and DNA-binding assays
exposure
Pre-reacted chromium cysteinate, chromium glutathione and chromium ascorbate preparations
limitations
These preparation-specific results challenge earlier assignments but do not show that Cr(VI) is harmless or directly reproduce every reductive chromate-DNA reaction.
nutrient_topic
Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
organism
Cell-free chemistry
plain_language
Pre-forming a metal complex can give a different result from reducing chromate in the presence of DNA; the claimed lesion identity needs checking.
primary_references
[chromium-p36662348] Examining the Potential Formation of Ternary DNA Complexes with Chromium‑Cysteine, Chromium-Ascorbate, and Chromium-Glutathione and Implications for Their Carcinogenicity. (2023). https://pubmed.ncbi.nlm.nih.gov/36662348/ DOI: 10.1007/s12011-023-03573-8
tissue_or_cell_type
Defined chromium complexes and DNA
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1186–1197
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Characterization of pre-reacted chromium-ligand preparations and DNA-binding assays · source_derived_draft · unverified_draft
### chromium-prereacted-dna-binding-null The characterized pre-reacted Cr(III)-cysteine, -glutathione and -ascorbate preparations did not measurably bind DNA or form the proposed ternary adducts under the tested conditions. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pre-forming a metal complex can give a different result from reducing chromate in the presence of DNA; the claimed lesion identity needs checking. organism: Cell-free chemistry tissue_or_cell_type: Defined chromium complexes and DNA experimental_model: Characterization of pre-reacted chromium-ligand preparations and DNA-binding assays limitations: These preparation-specific results challenge earlier assignments but do not show that Cr(VI) is harmless or directly reproduce every reductive chromate-DNA reaction. exposure: Pre-reacted chromium cysteinate, chromium glutathione and chromium ascorbate preparations evidence_span: {"source_cache": "artifacts/chromium-research/36662348.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "500f334d72ca34561016a11f0c3bf866998ee364085855e54a2f29025bc916a8", "start_char": 0, "end_char": 1155, "text_sha256": "500f334d72ca34561016a11f0c3bf866998ee364085855e54a2f29025bc916a8"} [chromium-p36662348] Examining the Potential Formation of Ternary DNA Complexes with Chromium‑Cysteine, Chromium-Ascorbate, and Chromium-Glutathione and Implications for Their Carcinogenicity. (2023). https://pubmed.ncbi.nlm.nih.gov/36662348/ DOI: 10.1007/s12011-023-03573-8
Complete structured claim and evidence
Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding.
Magnesium → Insulin receptor autophosphorylation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Magnesium -> insulin signaling -> carbohydrate handling.
experimental_model
Partially purified rat gastrocnemius receptors.
limitations
A depletion experiment; not isolated Mg binding to a particular receptor site.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Rattus norvegicus
plain_language
The receptor could still bind insulin, but its downstream activation was impaired.
primary_references
[mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
tissue_or_cell_type
Rat gastrocnemius receptor preparations and perfused hindquarter
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1503–1513
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified rat gastrocnemius receptors. · source_derived_draft · unverified_draft
### mg-deficiency-insr-autophosphorylation Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor could still bind insulin, but its downstream activation was impaired. organism: Rattus norvegicus tissue_or_cell_type: Rat gastrocnemius receptor preparations and perfused hindquarter experimental_model: Partially purified rat gastrocnemius receptors. limitations: A depletion experiment; not isolated Mg binding to a particular receptor site. cross_nutrient: Magnesium -> insulin signaling -> carbohydrate handling. [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
Complete structured claim and evidence
HLCS activates biotin with ATP to form enzyme-bound biotinyl-5-prime-AMP before transferring biotin to a carboxylase acceptor.
Human holocarboxylase synthetase / HLCS → Biotinyl-5-prime-AMP source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"}
experimental_model
Purified full-length and residue-58 human HLCS isoforms expressed in E. coli
exposure
Biotin/ATP activation and single-turnover biotin transfer
limitations
Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species.
nutrient_topic
Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
organism
Homo sapiens
plain_language
Biotin must first be activated before it can be attached to an enzyme.
primary_references
[b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
tissue_or_cell_type
Purified proteins and minimal biotin-accepting substrate
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 351–362
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified full-length and residue-58 human HLCS isoforms expressed in E. coli · source_derived_draft · unverified_draft
### b7-hlcs-adenylation HLCS activates biotin with ATP to form enzyme-bound biotinyl-5-prime-AMP before transferring biotin to a carboxylase acceptor. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin must first be activated before it can be attached to an enzyme. organism: Homo sapiens tissue_or_cell_type: Purified proteins and minimal biotin-accepting substrate experimental_model: Purified full-length and residue-58 human HLCS isoforms expressed in E. coli limitations: Minimal-substrate kinetics do not prove a universal tissue allocation hierarchy; expression host is not the protein species. exposure: Biotin/ATP activation and single-turnover biotin transfer evidence_span: {"source_cache": "artifacts/biotin-research/19740736.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d785655901465bc9798378986d954b87111e3bd73d6877d9d60ae3d95cac0a37", "start_char": 2587, "end_char": 3080, "text_sha256": "fa0ec838311a45e8ccebf38a73e340a46417eae6bc300064c1165a4a0b711889"} [b7-p19740736] Distinct amino termini of two human HCS isoforms influence biotin acceptor substrate recognition. (2009). https://pubmed.ncbi.nlm.nih.gov/19740736/ DOI: 10.1074/jbc.m109.046201
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

AMPK loss removes a chromium-picolinate response

Condition: machinery_impairment · Experimental AMPK depletion by siRNA in rat L6 myotubes.

Normal role: AMPK participates in the measured membrane and glucose-transport response.

Recorded consequence: Chromium picolinate no longer protected GLUT4 regulation and glucose transport.

Scope: Rat muscle cell culture; a machinery-dependence experiment, not chromium deficiency.

An altered carrier can change chromium delivery

Condition: machinery_impairment · Glycation of transferrin during glucose incubation; temperature/storage controls also alter binding.

Normal role: Transferrin can bind chromium and participate in its experimental distribution.

Recorded consequence: The modified preparation delivered less chromium to rat tissues.

Scope: Protein-preparation and rat experiments; reduced delivery is not a validated human deficiency syndrome.

Historical parenteral cases interpreted as chromium deficiency

Condition: nutrient_deficiency · Prolonged parenteral nutrition followed by glucose intolerance, weight loss and neurological findings.

Normal role: Insulin-responsive glucose utilization supports energy metabolism; the specific obligatory role of chromium remains uncertain.

Recorded consequence: Chromium addition was followed by improved glucose utilization and neurological findings in the reported cases.

Scope: Historical human case reports. The nutrient_deficiency category records the authors’ interpretation, not an established general dietary chromium-deficiency syndrome.

A chromium-free supplement does not guarantee chromium-free nutrition

Condition: biomarker_context · Parenteral nutrition formulated without intentional chromium supplementation.

Normal role: Circulating and urinary chromium reflect exposure and handling.

Recorded consequence: Plasma chromium increased with duration of parenteral nutrition despite no added chromium.

Scope: Premature infants; formulation, contamination and measured exposure are different concepts.

Low-chromium rat diets give context-dependent results

Condition: nutrient_deficiency · Experimental lower chromium intake in controlled rat diets.

Normal role: Glucose and lipid regulation have multiple nutrient and signaling inputs; a required chromium function remains disputed.

Recorded consequence: One model showed no glucose abnormality; another high-fat/high-sucrose model showed insulin and adiposity changes without higher glucose.

Scope: Separate rat strains, backgrounds and durations. Experimental low intake is not a validated human chromium-deficiency diagnosis.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Does chromium picolinate improve glycemic control in treated type 2 diabetes?The 1997 trial reported substantial HbA1c improvement, while the 2006 insulin-treated trial found approximately equal improvement with chromium and placebo. A smaller sulfonylurea trial reported benefit, and later work found heterogeneous responses. Dose, baseline glycemia, medication, population, analysis and study quality could contribute; no single verified mechanism explains the differences.Read the recorded disagreement
Is isolated chromodulin a pre-existing cellular chromium signal or an extraction product?Early isolation work interpreted a bovine-liver low-molecular-weight chromium fraction as a natural candidate for biologically active chromium. Later intact-cell versus lysate spectroscopy showed metal redistribution during extraction and a resulting chromodulin-like fraction, directly challenging that interpretation. The later experiments used Cr(VI)-exposed cells; the exposure and isolation conditions must remain visible.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

What is the molecular route for nutritional Cr(III) across human intestinal cells and from the transferrin endosome into the cytosol?Absorption and release assays are not a complete identification of the transport machinery. A plausible transferrin route does not identify an essential chromium-dependent enzyme.
Does chromium occupy an obligatory human insulin-signaling cofactor site?Chromodulin isolate activity, cell signaling responses and computational metal-site models do not establish an indispensable endogenous human cofactor. PMID 36220150 is an in-silico comparison with Fe, Mg and Zn, not a human competition experiment.
Can a blood, urine or hair chromium result diagnose an established nutritional deficiency?No validated general chromium-status test or clinically defined dietary deficiency state is established. Historical case-report reference ranges and supplement-responsive glucose measurements are not diagnostic cutoffs.
Which chromium–small-molecule–DNA structures account for mutagenicity in each reaction system?Reductive chromate/DNA experiments and pre-reacted Cr(III)-ligand experiments use different preparations. PMID 36662348 questions specific earlier ternary-adduct assignments; neither result should be generalized to every chromium complex or ordinary dietary exposure.
Are chromium compounds interchangeable in long-term human efficacy or safety?Oxidation state, ligand, route, retained dose and host context differ. The selected trials and cell experiments do not establish a class-wide benefit or long-term safety conclusion.
Do chromium–magnesium, chromium–biotin or chromium–vitamin-D combinations have reproducible interactions beyond their separate effects?Combination outcomes are recorded, but individual-component controls, between-group interaction tests, independent replication and dose/species comparability are needed before calling a universal synergy.
Does ordinary chromium supplementation impair human iron nutrition?Shared carrier chemistry and high-dose rat interactions are insufficient to establish this; the small older-men trial did not detect an adverse iron-status effect. Iron deficiency, overload and normal iron status cannot be merged.
Which signaling route predicts a response in a particular person?Membrane cholesterol/actin, AMPK and IRS-1/PI3K/PTP1B findings come from different experimental systems. They are possible routes, not a universally validated chromium → insulin-receptor → glucose-control sequence.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Chromium

The mechanisms

The tested picolinate form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.

AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model.

In obese insulin-resistant rats, chromium picolinate increased insulin-stimulated IRS-1 phosphorylation without increasing IRS protein abundance.

Obese rats receiving chromium picolinate had lower muscle PTP1B abundance and lower activity after correction for protein content.

At follow-up, the combined chromium-magnesium group had lower HOMA-IR and glycemic measures than the three other groups in the reported analysis.

The combination trial reported a between-group difference in HbA1c change (p=0.03); HbA1c fell 0.54 percentage points within the active-treatment group.

Chromium picolinate did not change the measured hematologic indices, serum iron or ferritin relative to placebo during the training study.

In the 1977 case, intravenous chromium was followed by normalization of the measured glucose-tolerance rate and respiratory quotient after two weeks, with insulin subsequently no longer required.

The six-month low-chromium diet did not alter glucose responses in glucose- or insulin-tolerance tests relative to the standard diet.

After four months, reported HbA1c values were 8.5%, 7.5% and 6.6% in the placebo, 200 µg/day and 1,000 µg/day groups, respectively.

HbA1c fell by about 0.4 percentage points in all three groups, with no chromium benefit over placebo.

Cr(III) uptake and vascular transfer were nonsaturable across 0.2–20 µmol/L in the perfused rat intestine; the authors interpreted the behavior as passive diffusion.

Estimated fractional chromium absorption fell from about 2% at 10 µg/day intake to about 0.5% at 40 µg/day in the study.

Rapid urinary loss accounted for much newly absorbed chromium picolinate; in the human comparison, seven-day retention was similarly low for picolinate and phenylalaninate.

Apparent absorption in the human comparison was about 0.8–1%, higher than the 0.04–0.24% range across the tested rat complexes.

Cr(III)-transferrin crystals contained a chromium-loaded closed C-terminal lobe and an open empty N-terminal lobe; two tyrosines, histidine, aspartate and chelating malonate coordinated the metal.

Acidic pH promoted rapid Cr(III) release from the weak transferrin site; release from the tighter site was slower and depended on the chelating environment.

Binding of chromium-loaded transferrin to soluble transferrin receptor accelerated chromium release from both sites at acidic pH.

A human chromium-transferrin conformation formed 5–60 minutes after loading released chromium rapidly at endosomal pH, whereas the slowly formed conformation used in many older assays released it slowly.

Insulin stimulated transferrin-associated chromium transport from blood into rat tissues, with liver and kidneys prominent destinations.

Insulin-associated urinary chromium loss increased alongside a low-molecular-weight fraction interpreted as probable chromodulin in the rat study.

The bovine-liver low-molecular-weight isolate contained approximately four Cr(III) ions per peptide, with spectra consistent with carboxylate-supported metal assemblies; one tetranuclear versus two dinuclear assemblies was unresolved.

Most Cr(III) formed in Cr(VI)-treated cells was associated with high-molecular-mass ligands; cell lysis redistributed chromium into a low-molecular-weight fraction spectroscopically similar to reported chromodulin.

The low-molecular-weight chromium-binding preparation bound insulin-activated rat insulin receptor with a reported dissociation constant near 250 pM.

Added chromium oligopeptide enhanced insulin-stimulated receptor tyrosine-kinase activity by up to eightfold in rat adipocyte membrane fragments; no enhancement occurred without insulin.

The preparation’s ability to enhance insulin-receptor tyrosine-kinase activity depended on its chromium content.

The isolate increased membrane phosphotyrosine-phosphatase activity in proportion to the amount added, while the isolate itself had no intrinsic phosphatase activity.

The tested chloride form mobilized GLUT4-containing vesicles toward the cell surface; insulin promoted their incorporation into the plasma membrane.

Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit.

Chromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps.

Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment.

Chromium picolinate protected hyperinsulinemic L6 myotubes against excess membrane cholesterol.

Chromium picolinate protected L6 myotubes from hyperinsulinemia-associated cortical filamentous-actin loss.

AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes.

Chromium picolinate increased insulin-stimulated PI3K activity in muscle from the obese rats without increasing PI3K protein abundance.

Chromium picolinate increased plasma-membrane CD36 localization in 3T3-L1 adipocytes; combining it with insulin did not produce additive CD36 translocation.

Glycated transferrin retained two chromium-binding equivalents but had altered spectroscopic behavior and greatly reduced chromium delivery in rats.

Chromium supplementation raised tissue chromium less strongly in iron-deficient rats than in rats with adequate iron.

High chromium-propionate supplementation did not deepen the measured adverse iron-status and hematologic changes from iron restriction.

High dietary iron reduced serum, liver and kidney chromium concentrations in the study.

Chromium supplementation reduced kidney iron with adequate dietary iron, but increasing chromium raised kidney iron when the background diet was iron-excessive.

Chromium picolinate did not alter the training-associated changes in total iron-binding capacity or transferrin saturation.

The chromium-plus-magnesium group had lower fasting glucose, fasting insulin and the reported insulin-resistance index than its own baseline; the individual-treatment groups lacked significant within-group changes.

GLUT4 mRNA increased 2.9-fold from baseline in activated T lymphocytes in the combined-treatment group.

GSK3β mRNA decreased 2.2-fold from baseline in activated T lymphocytes in the combined-treatment group.

The combined-treatment group had higher HDL cholesterol than the other groups in the reported analysis.

The zinc-magnesium-chromium regimen did not significantly improve measured metabolic-syndrome risk components, including serum glucose, relative to placebo.

The three-mineral regimen reduced serum CRP relative to placebo despite the lack of improvement in the measured metabolic-risk components.

HOMA-IR rose in the placebo and vitamin-D3-only groups but was controlled in the chromium and chromium-plus-vitamin-D3 groups.

TNF-alpha decreased in the vitamin-D3, chromium and combined-treatment groups.

HbA1c, fasting glucose and the lipid profile did not change significantly across the study’s groups.

Fasting glucose changed by −9.8 mg/dL with chromium picolinate plus biotin versus +0.7 mg/dL with placebo (p=0.02).

The chromium-histidinate-plus-biotin condition gave the highest reported GLUT1 protein levels among the compared high-fat-diet interventions in brain and liver.

The chromium-histidinate-plus-biotin condition gave the highest reported GLUT3 protein levels among the compared high-fat-diet interventions in brain and liver.

The chromium-histidinate-plus-biotin condition gave the highest reported IRS-1 protein levels among the compared high-fat-diet interventions in brain and liver.

The chromium-histidinate-plus-biotin condition gave the highest reported PPAR-gamma protein levels among the compared high-fat-diet interventions in brain and liver.

Chromium picolinate plus ferric ammonium citrate produced greater insulin-stimulated glucose uptake than ferric ammonium citrate alone in C2C12 cells.

The combination had a lower intracellular ROS assay signal than ferric ammonium citrate alone.

Chromium co-treatment increased GLUT4 levels relative to the iron-only condition, alongside higher PI3K and Akt phosphorylation ratios.

Chromium picolinate attenuated the pancreatic beta-cell apoptosis associated with iron excess in the rat experiment.

Chromium treatment countered the iron-associated reduction in pancreatic Bcl-2.

Chromium treatment countered the iron-associated increase in pancreatic Bax.

Chromium treatment countered the iron-associated increase in pancreatic cleaved caspase-9.

Oral coadministration of nicotinic acid with labeled chromium did not significantly alter chromium retention in the rat study.

Oral coadministration of glutathione with labeled chromium did not significantly alter chromium retention in the rat study.

Peripheral nerve conduction returned to normal over the subsequent five-month period in the 1977 parenteral-nutrition case.

Chromium addition was followed by improved glucose tolerance, reduced insulin requirements, weight gain and disappearance of a confusional state in the 1979 case.

Plasma chromium increased with longer parenteral-nutrition exposure even when the trace-mineral supplement contained no chromium.

The neonatal study found no relation of measured plasma or urinary chromium to its assessed laboratory parameters or morbidity.

Supplemented diets produced lower insulin-response areas after glucose challenge than the low-chromium diet, despite the lack of a glucose-tolerance defect.

The low-chromium group had higher fasting insulin and higher insulin at 30 and 60 minutes after glucose than the normal-chromium group, without a difference in glucose levels.

The low-chromium group consumed more energy later in the experiment and accumulated more body fat than the normal-chromium group.

Fasting triglycerides were higher in the low-chromium group than the normal-chromium group at the end of the rat experiment.

The 1,000 µg/day group had lower fasting glucose than placebo at two and four months; four-month values were 7.1 versus 8.8 mmol/L.

Fasting and two-hour insulin measurements decreased in both chromium-supplemented groups in the reported study.

The chromium-plus-sulfonylurea group showed improved measured insulin sensitivity and glucose control compared with the study’s sulfonylurea/placebo comparison.

Chromium did not consistently improve insulin action across the full phenotype range; response-defined subgroups differed in baseline insulin resistance and glycemia but not chromium status.

Subjects randomized to chromium had lower intramyocellular lipid measurements in the substudy.