Glucose tolerance

What acts on it

1. Melatonin worsened glucose tolerance in MTNR1B risk carriers, while the corresponding impairment was not significant in noncarriers.

   Melatonin → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/melatonin-research/42346809.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8e4b84650338084b0a878a3b06138c9ef65502d7f9b119877434421b5131bc6", "start_char": 0, "end_char": 1941, "text_sha256": "a8e4b84650338084b0a878a3b06138c9ef65502d7f9b119877434421b5131bc6"}

   experimental_model

   Randomized double-blind placebo-controlled crossover physiology trial

   exposure

   5 mg oral melatonin; five-day laboratory protocol

   limitations

   Small genotype-stratified acute study published in 2026. Stronger carrier findings are not a population-wide diabetes risk estimate or evidence about all chronic formulations.

   nutrient_topic

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

   organism

   21 healthy European-ancestry participants: 10 risk carriers, 11 noncarriers

   plain_language

   The recent controlled study found a genotype-dependent response.

   primary_references

   [melatonin-p42346809] Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With MTNR1B Diabetes Risk Variant. (2026). https://pubmed.ncbi.nlm.nih.gov/42346809/ DOI: 10.2337/dc26-0164

   tissue_or_cell_type

   Insulin-modified IV glucose test and beta-cell modeling

   Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1189–1200

   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 crossover physiology trial · source_derived_draft · unverified_draft

   ### melatonin-2026-glucose-carriers Melatonin worsened glucose tolerance in MTNR1B risk carriers, while the corresponding impairment was not significant in noncarriers. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The recent controlled study found a genotype-dependent response. organism: 21 healthy European-ancestry participants: 10 risk carriers, 11 noncarriers tissue_or_cell_type: Insulin-modified IV glucose test and beta-cell modeling experimental_model: Randomized double-blind placebo-controlled crossover physiology trial limitations: Small genotype-stratified acute study published in 2026. Stronger carrier findings are not a population-wide diabetes risk estimate or evidence about all chronic formulations. exposure: 5 mg oral melatonin; five-day laboratory protocol evidence_span: {"source_cache": "artifacts/melatonin-research/42346809.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8e4b84650338084b0a878a3b06138c9ef65502d7f9b119877434421b5131bc6", "start_char": 0, "end_char": 1941, "text_sha256": "a8e4b84650338084b0a878a3b06138c9ef65502d7f9b119877434421b5131bc6"} [melatonin-p42346809] Melatonin Impairs Glucose Tolerance, First-Phase Insulin Secretion, and Insulin Feedback Inhibition; Interaction With MTNR1B Diabetes Risk Variant. (2026). https://pubmed.ncbi.nlm.nih.gov/42346809/ DOI: 10.2337/dc26-0164

   Complete structured claim and evidence

2. Melatonin impaired glucose tolerance during both morning and evening challenges.

   Melatonin → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/melatonin-research/25197811.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2ed431f069ffbe6ace434aba258b90c154b1d07e4c6b92816cba26bb3b31c04", "start_char": 0, "end_char": 1466, "text_sha256": "a2ed431f069ffbe6ace434aba258b90c154b1d07e4c6b92816cba26bb3b31c04"}

   experimental_model

   Single-blind placebo-controlled glucose challenges

   exposure

   5 mg melatonin 15 minutes before 75 g OGTT at 09:00 or 21:00

   limitations

   Acute high-exposure challenge; not evidence that every bedtime regimen causes diabetes. Estimated mechanisms varied by time of day.

   nutrient_topic

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

   organism

   21 healthy young women

   plain_language

   Melatonin exposure close to carbohydrate intake can matter metabolically.

   primary_references

   [melatonin-p25197811] Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening. (2014). https://pubmed.ncbi.nlm.nih.gov/25197811/ DOI: 10.5665/sleep.4088

   tissue_or_cell_type

   Oral glucose tolerance in morning and evening

   Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1059–1070

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-blind placebo-controlled glucose challenges · source_derived_draft · unverified_draft

   ### melatonin-acute-glucose Melatonin impaired glucose tolerance during both morning and evening challenges. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Melatonin exposure close to carbohydrate intake can matter metabolically. organism: 21 healthy young women tissue_or_cell_type: Oral glucose tolerance in morning and evening experimental_model: Single-blind placebo-controlled glucose challenges limitations: Acute high-exposure challenge; not evidence that every bedtime regimen causes diabetes. Estimated mechanisms varied by time of day. exposure: 5 mg melatonin 15 minutes before 75 g OGTT at 09:00 or 21:00 evidence_span: {"source_cache": "artifacts/melatonin-research/25197811.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a2ed431f069ffbe6ace434aba258b90c154b1d07e4c6b92816cba26bb3b31c04", "start_char": 0, "end_char": 1466, "text_sha256": "a2ed431f069ffbe6ace434aba258b90c154b1d07e4c6b92816cba26bb3b31c04"} [melatonin-p25197811] Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening. (2014). https://pubmed.ncbi.nlm.nih.gov/25197811/ DOI: 10.5665/sleep.4088

   Complete structured claim and evidence

3. 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

4. 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

5. 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

6. Five depleted subjects had impaired oral glucose tolerance; two tested intravenously did not, and insulin-resistance tests were negative.

   Potassium → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   nutrient_deficiency Imported condition classification; unverified.

   experimental_model

   Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion.

   limitations

   Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result.

   nutrient_topic

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

   organism

   Human

   plain_language

   The measured glucose effect depended on the test and was mild.

   primary_references

   [gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544

   tissue_or_cell_type

   Systemic glucose regulation

   trigger_kind

   nutrient_deficiency Imported condition classification; unverified.

   Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 846–855

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. · source_derived_draft · unverified_draft

   ### k-human-depletion-route-boundary Five depleted subjects had impaired oral glucose tolerance; two tested intravenously did not, and insulin-resistance tests were negative. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured glucose effect depended on the test and was mild. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. limitations: Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result. [gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544

   Complete structured claim and evidence

7. The 12-week KCl pilot found no significant between-group improvement in primary glucose AUC or OGTT insulin measures.

   Potassium chloride → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   biomarker_context Imported condition classification; unverified.

   experimental_model

   Prediabetes pilot, 40 mEq/day KCl, 27 completers.

   limitations

   Underpowered pilot; absence of significance is not proof of no effect.

   nutrient_topic

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

   organism

   Human

   plain_language

   The trial did not establish better glucose tolerance.

   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

   Systemic glucose regulation

   trigger_kind

   biomarker_context Imported condition classification; unverified.

   Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 924–933

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prediabetes pilot, 40 mEq/day KCl, 27 completers. · source_derived_draft · unverified_draft

   ### k-pilot-ogtt-null The 12-week KCl pilot found no significant between-group improvement in primary glucose AUC or OGTT insulin measures. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not establish better glucose tolerance. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Prediabetes pilot, 40 mEq/day KCl, 27 completers. limitations: Underpowered pilot; absence of significance is not proof of no effect. [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

8. High-fat-diet mice colonised with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin were abrogated.

   Bacteroides fragilis → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"}

   experimental_model

   Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments

   exposure

   Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice

   limitations

   A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed.

   nutrient_topic

   Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin

   organism

   Human and mouse

   plain_language

   Putting the bacterium back removed the benefit, which is what makes this more than a correlation.

   primary_references

   [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4

   tissue_or_cell_type

   Gut lumen and intestinal epithelium

   Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 892–903

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments · source_derived_draft · unverified_draft

   ### metformin-bfragilis-colonisation High-fat-diet mice colonised with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin were abrogated. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Putting the bacterium back removed the benefit, which is what makes this more than a correlation. organism: Human and mouse tissue_or_cell_type: Gut lumen and intestinal epithelium experimental_model: Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments limitations: A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed. exposure: Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice evidence_span: {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"} [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4

   Complete structured claim and evidence

9. Transfer of faecal samples from metformin-treated donors to germ-free mice improved glucose tolerance in the recipients.

   Gut microbiota composition → Glucose tolerance source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"}

   experimental_model

   Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator

   exposure

   Metformin or placebo for 4 months in treatment-naive type 2 diabetes

   limitations

   The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction.

   nutrient_topic

   Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin

   organism

   Human and mouse

   plain_language

   Moving only the bacteria moved part of the benefit with them.

   primary_references

   [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345

   tissue_or_cell_type

   Gut microbiome

   Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 918–929

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator · source_derived_draft · unverified_draft

   ### metformin-microbiome-transfer Transfer of faecal samples from metformin-treated donors to germ-free mice improved glucose tolerance in the recipients. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Moving only the bacteria moved part of the benefit with them. organism: Human and mouse tissue_or_cell_type: Gut microbiome experimental_model: Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator limitations: The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction. exposure: Metformin or placebo for 4 months in treatment-naive type 2 diabetes evidence_span: {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"} [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345

   Complete structured claim and evidence