Fasting plasma glucose

What acts on it

1. The aMT6s change did not correlate with the post-atenolol blood-glucose change.

   Urinary 6-sulfatoxymelatonin excretion → Fasting plasma glucose source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/melatonin-research/26946962.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992", "start_char": 0, "end_char": 1191, "text_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992"}

   experimental_model

   Nine-week antihypertensive pharmacogenetic cohort analysis

   exposure

   Atenolol treatment; urinary aMT6s normalized to creatinine

   limitations

   Association study; absence of correlation is not proof of no biological role. It does not support a simple linear explanation of atenolol-related glucose changes by lost melatonin.

   nutrient_topic

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

   organism

   232 hypertensive participants reported as Caucasian in PEAR

   plain_language

   Two effects occurring together do not show that one caused the other.

   primary_references

   [melatonin-p26946962] Melatonin Pathway and Atenolol-Related Glucose Dysregulation: Is There a Correlation? (2016). https://pubmed.ncbi.nlm.nih.gov/26946962/ DOI: 10.1111/cts.12389

   tissue_or_cell_type

   Fasting blood glucose change, not an OGTT-derived tolerance index

   Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1254–1265

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine-week antihypertensive pharmacogenetic cohort analysis · source_derived_draft · unverified_draft

   ### melatonin-atenolol-correlation-null The aMT6s change did not correlate with the post-atenolol blood-glucose change. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two effects occurring together do not show that one caused the other. organism: 232 hypertensive participants reported as Caucasian in PEAR tissue_or_cell_type: Fasting blood glucose change, not an OGTT-derived tolerance index experimental_model: Nine-week antihypertensive pharmacogenetic cohort analysis limitations: Association study; absence of correlation is not proof of no biological role. It does not support a simple linear explanation of atenolol-related glucose changes by lost melatonin. exposure: Atenolol treatment; urinary aMT6s normalized to creatinine evidence_span: {"source_cache": "artifacts/melatonin-research/26946962.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992", "start_char": 0, "end_char": 1191, "text_sha256": "ad9bf60e8f57ef2ec9fe9e4b74b848b9cc0711fe00cf5a9959bf489dd9c8f992"} [melatonin-p26946962] Melatonin Pathway and Atenolol-Related Glucose Dysregulation: Is There a Correlation? (2016). https://pubmed.ncbi.nlm.nih.gov/26946962/ DOI: 10.1111/cts.12389

   Complete structured claim and evidence

2. Concentrated broccoli sprout extract lowered fasting glucose in obese patients with dysregulated type 2 diabetes in the reported subgroup.

   Broccoli sprout preparation, composition specified per study → Fasting plasma glucose source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"}

   experimental_model

   Network-guided preclinical work with a human intervention

   exposure

   Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup

   limitations

   Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed.

   nutrient_topic

   Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

   organism

   Hepatic cell/animal models and humans with type 2 diabetes

   plain_language

   The clinical response depended on the studied metabolic population.

   primary_references

   [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

   tissue_or_cell_type

   Glucose production and clinical glucose control

   Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1152–1163

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network-guided preclinical work with a human intervention · source_derived_draft · unverified_draft

   ### sulforaphane-diabetes-glucose Concentrated broccoli sprout extract lowered fasting glucose in obese patients with dysregulated type 2 diabetes in the reported subgroup. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The clinical response depended on the studied metabolic population. organism: Hepatic cell/animal models and humans with type 2 diabetes tissue_or_cell_type: Glucose production and clinical glucose control experimental_model: Network-guided preclinical work with a human intervention limitations: Model-based mechanism and clinical subgroup outcomes are distinct; no equivalence to metformin in patients is claimed. exposure: Concentrated broccoli sprout extract; obese dysregulated-diabetes subgroup evidence_span: {"source_cache": "artifacts/sulforaphane-research/28615356.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e", "start_char": 0, "end_char": 1106, "text_sha256": "65f64f5fa5e84a03d3ba4b647ce94a815fd3bd345486b726e7a54f1a813cab0e"} [sulforaphane-p28615356] Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. (2017). https://pubmed.ncbi.nlm.nih.gov/28615356/ DOI: 10.1126/scitranslmed.aah4477

   Complete structured claim and evidence

3. The mean glucose reduction versus placebo was 0.2 mmol/L (95% CI -0.44 to -0.01; P=0.04), below the prespecified 0.3 mmol/L target.

   Broccoli sprout preparation, composition specified per study → Fasting plasma glucose source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/sulforaphane-research/39929977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "525674c523bafc5e583bea8f2402f9e6dcf792c93b5af0c0f19d3aee15393a92", "start_char": 0, "end_char": 1849, "text_sha256": "525674c523bafc5e583bea8f2402f9e6dcf792c93b5af0c0f19d3aee15393a92"}

   experimental_model

   Randomized double-blind placebo-controlled trial with exploratory microbiome analysis

   exposure

   Daily broccoli sprout extract for 12 weeks

   limitations

   Primary target was 0.3 mmol/L; subgroup and microbiome results were exploratory and need confirmation.

   nutrient_topic

   Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study

   organism

   Human prediabetes; 35 extract and 39 placebo participants analyzed

   plain_language

   A small statistical signal did not meet the trial's planned target.

   primary_references

   [sulforaphane-p39929977] Effect of broccoli sprout extract and baseline gut microbiota on fasting blood glucose in prediabetes: a randomized, placebo-controlled trial. (2025). https://pubmed.ncbi.nlm.nih.gov/39929977/ DOI: 10.1038/s41564-025-01932-w

   tissue_or_cell_type

   Fasting glucose and serum exposure

   Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 1178–1189

   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 trial with exploratory microbiome analysis · source_derived_draft · unverified_draft

   ### sulforaphane-prediabetes-primary The mean glucose reduction versus placebo was 0.2 mmol/L (95% CI -0.44 to -0.01; P=0.04), below the prespecified 0.3 mmol/L target. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small statistical signal did not meet the trial's planned target. organism: Human prediabetes; 35 extract and 39 placebo participants analyzed tissue_or_cell_type: Fasting glucose and serum exposure experimental_model: Randomized double-blind placebo-controlled trial with exploratory microbiome analysis limitations: Primary target was 0.3 mmol/L; subgroup and microbiome results were exploratory and need confirmation. exposure: Daily broccoli sprout extract for 12 weeks evidence_span: {"source_cache": "artifacts/sulforaphane-research/39929977.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "525674c523bafc5e583bea8f2402f9e6dcf792c93b5af0c0f19d3aee15393a92", "start_char": 0, "end_char": 1849, "text_sha256": "525674c523bafc5e583bea8f2402f9e6dcf792c93b5af0c0f19d3aee15393a92"} [sulforaphane-p39929977] Effect of broccoli sprout extract and baseline gut microbiota on fasting blood glucose in prediabetes: a randomized, placebo-controlled trial. (2025). https://pubmed.ncbi.nlm.nih.gov/39929977/ DOI: 10.1038/s41564-025-01932-w

   Complete structured claim and evidence

4. 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

5. 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

6. Fasting glucose changed -1.1 versus +6.1 mg/dL with KCl versus placebo, a secondary endpoint difference (P=0.03).

   Potassium chloride → Fasting plasma glucose source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   biomarker_context Imported condition classification; unverified.

   experimental_model

   Same 12-week prediabetes pilot.

   limitations

   Small sample and multiple endpoints; no diabetes-prevention endpoint.

   nutrient_topic

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

   organism

   Human

   plain_language

   Fasting glucose worsened less in the supplemented group.

   primary_references

   [chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570

   tissue_or_cell_type

   Blood

   trigger_kind

   biomarker_context Imported condition classification; unverified.

   Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 935–944

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same 12-week prediabetes pilot. · source_derived_draft · unverified_draft

   ### k-pilot-fasting-glucose Fasting glucose changed -1.1 versus +6.1 mg/dL with KCl versus placebo, a secondary endpoint difference (P=0.03). Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fasting glucose worsened less in the supplemented group. organism: Human tissue_or_cell_type: Blood experimental_model: Same 12-week prediabetes pilot. limitations: Small sample and multiple endpoints; no diabetes-prevention endpoint. [chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570

   Complete structured claim and evidence

7. Fasting plasma glucose and HbA1c levels were lower in KK-Ay mice fed 0.3% acetic acid for 8 weeks than in control mice, and acetic acid also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by AMP-activated protein kinase in the liver.

   Acetic acid → Fasting plasma glucose source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/acetate-research/16630552.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea", "start_char": 0, "end_char": 914, "text_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea"}

   experimental_model

   KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments

   exposure

   0.3% dietary acetic acid for 8 weeks; sodium acetate as neutralised acetic acid applied to rat hepatocytes

   limitations

   The hepatocyte arm used the neutralised salt and still activated AMPK, which does not sit easily beside the human finding that the acid rather than the salt lowered glucose. Both are recorded.

   nutrient_topic

   Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid

   organism

   Mouse

   plain_language

   Eight weeks of dietary acid lowered fasting glucose and long-term glucose control, and turned down the liver genes that make glucose and fat.

   primary_references

   [acetate-p16630552] Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16630552/ DOI: 10.1016/j.bbrc.2006.03.176

   tissue_or_cell_type

   Liver

   Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 407–418

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments · source_derived_draft · unverified_draft

   ### acetate-acetic-acid-ampk Fasting plasma glucose and HbA1c levels were lower in KK-Ay mice fed 0.3% acetic acid for 8 weeks than in control mice, and acetic acid also reduced the expression of genes involved in gluconeogenesis and lipogenesis, which is in part regulated by AMP-activated protein kinase in the liver. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Eight weeks of dietary acid lowered fasting glucose and long-term glucose control, and turned down the liver genes that make glucose and fat. organism: Mouse tissue_or_cell_type: Liver experimental_model: KK-Ay diabetic mice fed for 8 weeks, with rat hepatocyte experiments limitations: The hepatocyte arm used the neutralised salt and still activated AMPK, which does not sit easily beside the human finding that the acid rather than the salt lowered glucose. Both are recorded. exposure: 0.3% dietary acetic acid for 8 weeks; sodium acetate as neutralised acetic acid applied to rat hepatocytes evidence_span: {"source_cache": "artifacts/acetate-research/16630552.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea", "start_char": 0, "end_char": 914, "text_sha256": "8e99fe94e17c850602d0da9607212293dfc8d773e356b73ef37c4b071bbeabea"} [acetate-p16630552] Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice. (2006). https://pubmed.ncbi.nlm.nih.gov/16630552/ DOI: 10.1016/j.bbrc.2006.03.176

   Complete structured claim and evidence