Component
Energy intake / food intake
Energy intake / food intake. Species, exposure and limitations are retained in each linked claim.
1 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.
Where it participates (unsigned role)
Metformin prevented high-fat-diet weight gain in wild-type mice but not in mice lacking GDF15 or its receptor GFRAL, and a GFRAL-antagonist antibody reversed the weight effect in obese mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/31875646.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a25b31ade3977aabe24159b0374c42fe4fb48ab1464ba9ae69c73e63f41e742a", "start_char": 0, "end_char": 1454, "text_sha256": "a25b31ade3977aabe24159b0374c42fe4fb48ab1464ba9ae69c73e63f41e742a"}
- experimental_model
- Two randomised controlled trials in people plus wild-type, Gdf15-null and Gfral-null mice
- exposure
- Oral metformin; high-fat diet in mice; GFRAL-antagonist antibody
- limitations
- The weight mechanism is separable from the glucose mechanism in this work; the mouse knockouts carry the causal claim, the human trials the GDF15 rise. A publisher correction was issued for this paper (Nature 2020;578:E24, PMID 32051582); 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 and mouse
- plain_language
- The weight effect travelled through that hormone and its brainstem receptor.
- primary_references
- [metformin-p31875646] GDF15 mediates the effects of metformin on body weight and energy balance. (2020). https://pubmed.ncbi.nlm.nih.gov/31875646/ DOI: 10.1038/s41586-019-1911-y
- tissue_or_cell_type
- Distal intestine, kidney and brainstem receptor
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 788–799
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two randomised controlled trials in people plus wild-type, Gdf15-null and Gfral-null mice · source_derived_draft · unverified_draft
### metformin-gdf15-weight Metformin prevented high-fat-diet weight gain in wild-type mice but not in mice lacking GDF15 or its receptor GFRAL, and a GFRAL-antagonist antibody reversed the weight effect in obese mice. 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 weight effect travelled through that hormone and its brainstem receptor. organism: Human and mouse tissue_or_cell_type: Distal intestine, kidney and brainstem receptor experimental_model: Two randomised controlled trials in people plus wild-type, Gdf15-null and Gfral-null mice limitations: The weight mechanism is separable from the glucose mechanism in this work; the mouse knockouts carry the causal claim, the human trials the GDF15 rise. A publisher correction was issued for this paper (Nature 2020;578:E24, PMID 32051582); its notice body was not available, so its impact on these records has not been assessed. exposure: Oral metformin; high-fat diet in mice; GFRAL-antagonist antibody evidence_span: {"source_cache": "artifacts/metformin-research/31875646.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a25b31ade3977aabe24159b0374c42fe4fb48ab1464ba9ae69c73e63f41e742a", "start_char": 0, "end_char": 1454, "text_sha256": "a25b31ade3977aabe24159b0374c42fe4fb48ab1464ba9ae69c73e63f41e742a"} [metformin-p31875646] GDF15 mediates the effects of metformin on body weight and energy balance. (2020). https://pubmed.ncbi.nlm.nih.gov/31875646/ DOI: 10.1038/s41586-019-1911-y
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.