Evidence mapPaperPMID 33510216Full record

ArticleScientific reports2021

Inhibition of mitochondrial function by metformin increases glucose uptake, glycolysis and GDF-15 release from intestinal cells.

Ming Yang, Tamana Darwish, Pierre Larraufie, Debra Rimmington, Irene Cimino, Deborah A Goldspink, Benjamin Jenkins, Albert Koulman, Cheryl A Brighton, Marcella Ma and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
13.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 101 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Metformin Alone and in Combinations Alter the Methylation Patterns ofEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  7. Article
  8. Article
  9. N-Lactoyl Amino Acids: Emerging Biomarkers in Metabolism and Disease.Diabetes/metabolism research and reviews · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Ming YangMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Tamana DarwishMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Pierre LarraufieMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Debra RimmingtonMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Irene CiminoMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Deborah A GoldspinkMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Benjamin JenkinsMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Albert KoulmanMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Cheryl A BrightonMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Marcella MaMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Brian Y H LamMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Anthony P CollMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Stephen O'RahillyMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
Frank ReimannMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK. fr222@cam.ac.uk.
Fiona M GribbleMRC Metabolic Diseases Unit, Addenbrooke's Hospital, Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK. fmg23@cam.ac.uk.
University of Cambridge · GBWellcome Trust · GBAddenbrooke's Hospital · GBWellcome/MRC Institute of Metabolic Science · GB

Funding

Medical Research Council MC_UU_00014/1Medical Research Council MC_UU_00014/3Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/1Medical Research Council MC_UU_12012/3Medical Research Council MC_UU_12012/5MRC MC_UU_00014/1MRC MRC_MC_UU_12012/3Wellcome TrustWellcome Trust 100574/Z/12/ZWellcome Trust 106262/Z/14/ZWellcome Trust 106263/Z/14/Z
6 · The paper itself

Abstract

Even though metformin is widely used to treat type2 diabetes, reducing glycaemia and body weight, the mechanisms of action are still elusive. Recent studies have identified the gastrointestinal tract as an important site of action. Here we used intestinal organoids to explore the effects of metformin on intestinal cell physiology. Bulk RNA-sequencing analysis identified changes in hexose metabolism pathways, particularly glycolytic genes. Metformin increased expression of Slc2a1 (GLUT1), decreased expression of Slc2a2 (GLUT2) and Slc5a1 (SGLT1) whilst increasing GLUT-dependent glucose uptake and glycolytic rate as observed by live cell imaging of genetically encoded metabolite sensors and measurement of oxygen consumption and extracellular acidification rates. Metformin caused mitochondrial dysfunction and metformin's effects on 2D-cultures were phenocopied by treatment with rotenone and antimycin-A, including upregulation of GDF15 expression, previously linked to metformin dependent weight loss. Gene expression changes elicited by metformin were replicated in 3D apical-out organoids and distal small intestines of metformin treated mice. We conclude that metformin affects glucose uptake, glycolysis and GDF-15 secretion, likely downstream of the observed mitochondrial dysfunction. This may explain the effects of metformin on intestinal glucose utilisation and food balance.

Indexed as

AnimalsBiological TransportCell RespirationCells, CulturedComputational BiologyGene Expression ProfilingGlucoseGlucose Transport Proteins, FacilitativeGlycolysisGrowth Differentiation Factor 15Intestinal MucosaMaleMetforminMiceMitochondriaOxidative PhosphorylationGlucoseGlucose Transport Proteins, FacilitativeGrowth Differentiation Factor 15Metformin

Identifiers

PMID33510216
PMCPMC7843649
OpenAlexW3121734616

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.