Insulin-stimulated glucose uptake

What acts on it

1. Mg-deficient rat muscle had lower glucose uptake at submaximal insulin; basal and maximal-insulin uptake were preserved.

   Magnesium → Insulin-stimulated glucose uptake source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   nutrient_deficiency Imported condition classification; unverified.

   cross_nutrient

   Magnesium/insulin/glucose; impaired sensitivity is distinct from absence of transport.

   experimental_model

   Perfused rat hindquarter.

   limitations

   Muscle GLUT4 abundance was similar; the experiment does not establish a single causal intermediate.

   nutrient_topic

   Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

   organism

   Rattus norvegicus

   plain_language

   The response became less sensitive rather than completely stopping.

   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 1515–1525

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused rat hindquarter. · source_derived_draft · unverified_draft

   ### mg-deficiency-muscle-insulin-response Mg-deficient rat muscle had lower glucose uptake at submaximal insulin; basal and maximal-insulin uptake were preserved. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response became less sensitive rather than completely stopping. organism: Rattus norvegicus tissue_or_cell_type: Rat gastrocnemius receptor preparations and perfused hindquarter experimental_model: Perfused rat hindquarter. limitations: Muscle GLUT4 abundance was similar; the experiment does not establish a single causal intermediate. cross_nutrient: Magnesium/insulin/glucose; impaired sensitivity is distinct from absence of transport. [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

2. 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

3. 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

4. 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

5. Insulin-stimulated glucose disposal per kg fat-free mass increased by 25±7% after ten weeks of NMN, while the placebo group showed no corresponding change.

   NMN → Insulin-stimulated glucose uptake source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   Insulin (test_signal)

   evidence_span

   {"source_cache": "artifacts/niacin-clinical-sources/yoshino2021.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "e4999dc5b9d3392d8180280727c424044b35249bb24c999c3bc863cd23e6c856", "start_char": 6120, "end_char": 7140, "text_sha256": "152262160f005f7aac5e078287acca1db556d35a8645d8892492723992dec2dc"}

   experimental_model

   Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed

   exposure

   NMN 250 mg/day for 10 weeks; 13 NMN and 12 placebo participants

   limitations

   Small selected female cohort. Tissue NAD concentration, NAD turnover and clinical outcomes differ. No lifespan or diabetes-prevention endpoint. Positive muscle findings do not establish whole-body or cross-population benefit.

   nutrient_topic

   Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

   organism

   Homo sapiens

   plain_language

   In this small group of women, muscle responded better to insulin during the clamp test.

   primary_references

   [nia-clin-yoshino2021] Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. (2021). https://pubmed.ncbi.nlm.nih.gov/33888596/ DOI: 10.1126/science.abe9985

   tissue_or_cell_type

   Skeletal muscle, PBMCs, liver and adipose insulin sensitivity

   Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1487–1499

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed · source_derived_draft · unverified_draft

   ### nia-clin-nmn-muscle-insulin Insulin-stimulated glucose disposal per kg fat-free mass increased by 25±7% after ten weeks of NMN, while the placebo group showed no corresponding change. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this small group of women, muscle responded better to insulin during the clamp test. organism: Homo sapiens tissue_or_cell_type: Skeletal muscle, PBMCs, liver and adipose insulin sensitivity experimental_model: Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed limitations: Small selected female cohort. Tissue NAD concentration, NAD turnover and clinical outcomes differ. No lifespan or diabetes-prevention endpoint. Positive muscle findings do not establish whole-body or cross-population benefit. exposure: NMN 250 mg/day for 10 weeks; 13 NMN and 12 placebo participants cross_nutrient: Insulin (test_signal) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/yoshino2021.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "e4999dc5b9d3392d8180280727c424044b35249bb24c999c3bc863cd23e6c856", "start_char": 6120, "end_char": 7140, "text_sha256": "152262160f005f7aac5e078287acca1db556d35a8645d8892492723992dec2dc"} [nia-clin-yoshino2021] Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. (2021). https://pubmed.ncbi.nlm.nih.gov/33888596/ DOI: 10.1126/science.abe9985

   Complete structured claim and evidence

6. Twelve weeks of NR did not improve clamp insulin sensitivity, glucose production or disposal, lipid mobilization, resting energy expenditure or body composition in this trial.

   Nicotinamide riboside → Insulin-stimulated glucose uptake source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   Niacin precursor form and the measured endpoint are separate graph entities.

   evidence_span

   {"source_cache": "artifacts/niacin-clinical-sources/dollerup2018.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "dd5668627aa4f11bce6460dd6d163248c711dd43b85b6265a4055cf96012b241", "start_char": 0, "end_char": 1987, "text_sha256": "dd5668627aa4f11bce6460dd6d163248c711dd43b85b6265a4055cf96012b241"}

   experimental_model

   Randomized double-blind trial; 40 sedentary obese insulin-resistant men aged 40–70

   exposure

   NR 1,000 mg twice daily versus placebo for 12 weeks

   limitations

   Different precursor and population from the NMN female trial. No efficacy demonstrated for the tested endpoints; short tolerability observations do not establish universal long-term safety.

   nutrient_topic

   Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

   organism

   Homo sapiens

   plain_language

   NR did not produce a general metabolic improvement in these insulin-resistant men.

   primary_references

   [nia-clin-dollerup2018] A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. (2018). https://pubmed.ncbi.nlm.nih.gov/29992272/ DOI: 10.1093/ajcn/nqy132

   tissue_or_cell_type

   Clamp glucose metabolism and body composition

   Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1543–1555

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial; 40 sedentary obese insulin-resistant men aged 40–70 · source_derived_draft · unverified_draft

   ### nia-clin-nr-obese-men Twelve weeks of NR did not improve clamp insulin sensitivity, glucose production or disposal, lipid mobilization, resting energy expenditure or body composition in this trial. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: NR did not produce a general metabolic improvement in these insulin-resistant men. organism: Homo sapiens tissue_or_cell_type: Clamp glucose metabolism and body composition experimental_model: Randomized double-blind trial; 40 sedentary obese insulin-resistant men aged 40–70 limitations: Different precursor and population from the NMN female trial. No efficacy demonstrated for the tested endpoints; short tolerability observations do not establish universal long-term safety. exposure: NR 1,000 mg twice daily versus placebo for 12 weeks cross_nutrient: Niacin precursor form and the measured endpoint are separate graph entities. evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/dollerup2018.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "dd5668627aa4f11bce6460dd6d163248c711dd43b85b6265a4055cf96012b241", "start_char": 0, "end_char": 1987, "text_sha256": "dd5668627aa4f11bce6460dd6d163248c711dd43b85b6265a4055cf96012b241"} [nia-clin-dollerup2018] A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. (2018). https://pubmed.ncbi.nlm.nih.gov/29992272/ DOI: 10.1093/ajcn/nqy132

   Complete structured claim and evidence

7. Adipocytes treated with 8-methyl nonanoic acid during 5-day maturation exhibited a reduced lipolytic response to isoproterenol and an increased glucose uptake when stimulated with insulin.

   8-methyl nonanoic acid, the methyl-branched medium-chain fatty acid released from dihydrocapsaicin → Insulin-stimulated glucose uptake source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/dihydrocapsaicin-research/36681810.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14c4f7752262c5a27fb7b848664015595f598cb51edcc2d5df96f1140be143cb", "start_char": 0, "end_char": 1600, "text_sha256": "14c4f7752262c5a27fb7b848664015595f598cb51edcc2d5df96f1140be143cb"}

   experimental_model

   3T3-L1 adipocytes assayed for viability, lipid accumulation, AMPK activity, lipolysis and glucose uptake

   exposure

   8-methyl nonanoic acid applied during 48-hour nutrient starvation or 5-day maturation

   limitations

   A cell-line study of the metabolite. The two exposure windows give different effects, which is recorded rather than averaged.

   nutrient_topic

   Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

   organism

   Mouse cells

   plain_language

   Given while the fat cells mature, it makes them take up more glucose and release less fat on demand.

   primary_references

   [dhc-p36681810] Cellular responses to 8-methyl nonanoic acid, a degradation by-product of dihydrocapsaicin, in 3T3-L1 adipocytes. (2023). https://pubmed.ncbi.nlm.nih.gov/36681810/ DOI: 10.1186/s12906-023-03844-w

   tissue_or_cell_type

   Adipocytes

   Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 634–645

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 3T3-L1 adipocytes assayed for viability, lipid accumulation, AMPK activity, lipolysis and glucose uptake · source_derived_draft · unverified_draft

   ### dhc-8-mna-maturation-effects Adipocytes treated with 8-methyl nonanoic acid during 5-day maturation exhibited a reduced lipolytic response to isoproterenol and an increased glucose uptake when stimulated with insulin. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Given while the fat cells mature, it makes them take up more glucose and release less fat on demand. organism: Mouse cells tissue_or_cell_type: Adipocytes experimental_model: 3T3-L1 adipocytes assayed for viability, lipid accumulation, AMPK activity, lipolysis and glucose uptake limitations: A cell-line study of the metabolite. The two exposure windows give different effects, which is recorded rather than averaged. exposure: 8-methyl nonanoic acid applied during 48-hour nutrient starvation or 5-day maturation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/36681810.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14c4f7752262c5a27fb7b848664015595f598cb51edcc2d5df96f1140be143cb", "start_char": 0, "end_char": 1600, "text_sha256": "14c4f7752262c5a27fb7b848664015595f598cb51edcc2d5df96f1140be143cb"} [dhc-p36681810] Cellular responses to 8-methyl nonanoic acid, a degradation by-product of dihydrocapsaicin, in 3T3-L1 adipocytes. (2023). https://pubmed.ncbi.nlm.nih.gov/36681810/ DOI: 10.1186/s12906-023-03844-w

   Complete structured claim and evidence