Component
Gluconeogenesis from lactate and glycerol
Gluconeogenesis from lactate and glycerol. 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
The altered hepatocellular redox state reduced the conversion of lactate and glycerol to glucose and decreased hepatic gluconeogenesis.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/24847880.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8378baac19afd12fd3ca66206d079db20e7229a9295414e9678979352e10d92b", "start_char": 0, "end_char": 1499, "text_sha256": "8378baac19afd12fd3ca66206d079db20e7229a9295414e9678979352e10d92b"}
- experimental_model
- Rat antisense-oligonucleotide knockdown, whole-body knockout mice and hepatic redox measurements
- exposure
- Acute and chronic low-dose metformin; mGPD knockdown and knockout
- limitations
- A redox-shuttle mechanism established in rodents at low doses; it does not by itself exclude complex I or AMPK contributions in other tissues.
- nutrient_topic
- Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
- organism
- Rat and mouse
- plain_language
- Two of the raw materials for making new glucose can no longer be used.
- primary_references
- [metformin-p24847880] Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. (2014). https://pubmed.ncbi.nlm.nih.gov/24847880/ DOI: 10.1038/nature13270
- tissue_or_cell_type
- Liver
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 489–500
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat antisense-oligonucleotide knockdown, whole-body knockout mice and hepatic redox measurements · source_derived_draft · unverified_draft
### metformin-mgpd-gluconeogenesis The altered hepatocellular redox state reduced the conversion of lactate and glycerol to glucose and decreased hepatic gluconeogenesis. 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: Two of the raw materials for making new glucose can no longer be used. organism: Rat and mouse tissue_or_cell_type: Liver experimental_model: Rat antisense-oligonucleotide knockdown, whole-body knockout mice and hepatic redox measurements limitations: A redox-shuttle mechanism established in rodents at low doses; it does not by itself exclude complex I or AMPK contributions in other tissues. exposure: Acute and chronic low-dose metformin; mGPD knockdown and knockout evidence_span: {"source_cache": "artifacts/metformin-research/24847880.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8378baac19afd12fd3ca66206d079db20e7229a9295414e9678979352e10d92b", "start_char": 0, "end_char": 1499, "text_sha256": "8378baac19afd12fd3ca66206d079db20e7229a9295414e9678979352e10d92b"} [metformin-p24847880] Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. (2014). https://pubmed.ncbi.nlm.nih.gov/24847880/ DOI: 10.1038/nature13270
Complete structured claim and evidence
Where it participates (unsigned role)
The authors concluded that suppression of accelerated basal hepatic glucose production was most likely secondary to an inhibition of hepatic glycogenolysis, since the percentage of gluconeogenesis from lactate and the rate of lactate-derived gluconeogenesis were unchanged.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/8923861.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "164b296465a3d5730d3dba4c66062ce97c227e61b866b6a42c5beb772f51d688", "start_char": 0, "end_char": 3516, "text_sha256": "164b296465a3d5730d3dba4c66062ce97c227e61b866b6a42c5beb772f51d688"}
- experimental_model
- Randomised double-blind placebo-controlled trial with tracer infusions and euglycaemic clamp
- exposure
- 15 weeks of metformin versus placebo in 20 people with type 2 diabetes
- limitations
- Tracer measurement of where the glucose effect comes from. Lactate turnover was measured directly and did not change, which bears on lactate safety questions.
- 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 reduction came from breaking down stored glycogen less, not from making less new glucose.
- primary_references
- [metformin-p8923861] Metabolic effects of metformin on glucose and lactate metabolism in noninsulin-dependent diabetes mellitus. (1996). https://pubmed.ncbi.nlm.nih.gov/8923861/ DOI: 10.1210/jcem.81.11.8923861
- tissue_or_cell_type
- Liver and whole body
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1399–1410
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised double-blind placebo-controlled trial with tracer infusions and euglycaemic clamp · source_derived_draft · unverified_draft
### metformin-human-glycogenolysis The authors concluded that suppression of accelerated basal hepatic glucose production was most likely secondary to an inhibition of hepatic glycogenolysis, since the percentage of gluconeogenesis from lactate and the rate of lactate-derived gluconeogenesis were unchanged. 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 reduction came from breaking down stored glycogen less, not from making less new glucose. organism: Human tissue_or_cell_type: Liver and whole body experimental_model: Randomised double-blind placebo-controlled trial with tracer infusions and euglycaemic clamp limitations: Tracer measurement of where the glucose effect comes from. Lactate turnover was measured directly and did not change, which bears on lactate safety questions. exposure: 15 weeks of metformin versus placebo in 20 people with type 2 diabetes evidence_span: {"source_cache": "artifacts/metformin-research/8923861.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "164b296465a3d5730d3dba4c66062ce97c227e61b866b6a42c5beb772f51d688", "start_char": 0, "end_char": 3516, "text_sha256": "164b296465a3d5730d3dba4c66062ce97c227e61b866b6a42c5beb772f51d688"} [metformin-p8923861] Metabolic effects of metformin on glucose and lactate metabolism in noninsulin-dependent diabetes mellitus. (1996). https://pubmed.ncbi.nlm.nih.gov/8923861/ DOI: 10.1210/jcem.81.11.8923861
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.