Component
Gastrointestinal intolerance of metformin
Gastrointestinal intolerance of metformin. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Carriage of two reduced-function OCT1 alleles was associated with metformin intolerance (odds ratio 2.41), rising to 4.13 in people also taking OCT1-inhibiting drugs.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/25510240.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8eaf94237679ed7436f863e210d17b13a7219d064e46e7da915ed083c5b04c9", "start_char": 0, "end_char": 1355, "text_sha256": "f8eaf94237679ed7436f863e210d17b13a7219d064e46e7da915ed083c5b04c9"}
- experimental_model
- Case-control comparison of 251 metformin-intolerant and 1915 tolerant people in GoDARTS
- exposure
- Prescribed metformin, OCT1 genotype and co-prescribed OCT1 inhibitors
- limitations
- An association study. Intolerance is self-evidently multifactorial, and the proposed intestinal-concentration mechanism was not measured here.
- 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
- plain_language
- The transporter that controls where the drug goes is also linked to who cannot tolerate it.
- primary_references
- [metformin-p25510240] Association of Organic Cation Transporter 1 With Intolerance to Metformin in Type 2 Diabetes: A GoDARTS Study. (2015). https://pubmed.ncbi.nlm.nih.gov/25510240/ DOI: 10.2337/db14-1388
- tissue_or_cell_type
- Gastrointestinal tolerance
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 359–370
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case-control comparison of 251 metformin-intolerant and 1915 tolerant people in GoDARTS · source_derived_draft · unverified_draft
### metformin-oct1-intolerance Carriage of two reduced-function OCT1 alleles was associated with metformin intolerance (odds ratio 2.41), rising to 4.13 in people also taking OCT1-inhibiting drugs. 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: The transporter that controls where the drug goes is also linked to who cannot tolerate it. organism: Human tissue_or_cell_type: Gastrointestinal tolerance experimental_model: Case-control comparison of 251 metformin-intolerant and 1915 tolerant people in GoDARTS limitations: An association study. Intolerance is self-evidently multifactorial, and the proposed intestinal-concentration mechanism was not measured here. exposure: Prescribed metformin, OCT1 genotype and co-prescribed OCT1 inhibitors evidence_span: {"source_cache": "artifacts/metformin-research/25510240.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8eaf94237679ed7436f863e210d17b13a7219d064e46e7da915ed083c5b04c9", "start_char": 0, "end_char": 1355, "text_sha256": "f8eaf94237679ed7436f863e210d17b13a7219d064e46e7da915ed083c5b04c9"} [metformin-p25510240] Association of Organic Cation Transporter 1 With Intolerance to Metformin in Type 2 Diabetes: A GoDARTS Study. (2015). https://pubmed.ncbi.nlm.nih.gov/25510240/ DOI: 10.2337/db14-1388
Complete structured claim and evidence
Where it participates (unsigned role)
A relative increase in the abundance of Escherichia species was proposed as a microbiota-mediated mechanism behind the known intestinal adverse effects of metformin.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/26633628.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f83ac1daddf6372ef8d16d3944ed9b6d62f0d1c12fb5815fb7c27cda2244f984", "start_char": 0, "end_char": 1570, "text_sha256": "f83ac1daddf6372ef8d16d3944ed9b6d62f0d1c12fb5815fb7c27cda2244f984"}
- experimental_model
- Reanalysis of 784 human gut metagenomes stratified by treatment
- exposure
- Metformin treatment as a confounder in type 2 diabetes metagenomes
- limitations
- An observational reanalysis. It separates disease signature from drug signature; it does not measure a clinical outcome. A corrigendum was issued for this paper (Nature 2017;545:116, PMID 28470190); its notice body was not available, so its impact on these records has not been assessed.
- 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
- plain_language
- The same shift may explain why the drug upsets some people’s gut.
- primary_references
- [metformin-p26633628] Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota. (2015). https://pubmed.ncbi.nlm.nih.gov/26633628/ DOI: 10.1038/nature15766
- tissue_or_cell_type
- Gut microbiome
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 957–968
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reanalysis of 784 human gut metagenomes stratified by treatment · source_derived_draft · unverified_draft
### metformin-escherichia-increase A relative increase in the abundance of Escherichia species was proposed as a microbiota-mediated mechanism behind the known intestinal adverse effects of metformin. 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: The same shift may explain why the drug upsets some people’s gut. organism: Human tissue_or_cell_type: Gut microbiome experimental_model: Reanalysis of 784 human gut metagenomes stratified by treatment limitations: An observational reanalysis. It separates disease signature from drug signature; it does not measure a clinical outcome. A corrigendum was issued for this paper (Nature 2017;545:116, PMID 28470190); its notice body was not available, so its impact on these records has not been assessed. exposure: Metformin treatment as a confounder in type 2 diabetes metagenomes evidence_span: {"source_cache": "artifacts/metformin-research/26633628.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f83ac1daddf6372ef8d16d3944ed9b6d62f0d1c12fb5815fb7c27cda2244f984", "start_char": 0, "end_char": 1570, "text_sha256": "f83ac1daddf6372ef8d16d3944ed9b6d62f0d1c12fb5815fb7c27cda2244f984"} [metformin-p26633628] Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota. (2015). https://pubmed.ncbi.nlm.nih.gov/26633628/ DOI: 10.1038/nature15766
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.