Evidence mapPaperPMID 36809274Full record

ArticleJCI insight2023

Mapping the metabolic reprogramming induced by sodium-glucose cotransporter 2 inhibition.

Aviram Kogot-Levin, Yael Riahi, Ifat Abramovich, Ofri Mosenzon, Bella Agranovich, Liat Kadosh, Rachel Ben-Haroush Schyr, Doron Kleiman, Liad Hinden, Erol Cerasi and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
11.7field-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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  3. Article
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  6. Article
  7. SGLT2 inhibitors and acute kidney injury.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. METTL3 mediates atheroprone flow-induced glycolysis in endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
  15. Sodium-glucose cotransporter-2 inhibitors protect tissuesWorld journal of experimental medicine · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 5 institutions in 3 countries.

Aviram Kogot-LevinDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Yael RiahiDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Ifat AbramovichThe laboratory for Metabolism in Health and Disease, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology Haifa, Israel.
Ofri MosenzonDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Bella AgranovichThe laboratory for Metabolism in Health and Disease, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology Haifa, Israel.
Liat KadoshDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Rachel Ben-Haroush SchyrDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada, Faculty of Medicine, and.
Doron KleimanDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada, Faculty of Medicine, and.
Liad HindenObesity and Metabolism Laboratory, Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Erol CerasiDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Danny Ben-ZviDepartment of Developmental Biology and Cancer Research, Institute of Medical Research Israel-Canada, Faculty of Medicine, and.
Ernesto Bernal-MizrachiDepartment of Internal Medicine, Division of Endocrinology, Metabolism and Diabetes, Miller School of Medicine, University of Miami, Miami, Florida, USA.
Joseph TamObesity and Metabolism Laboratory, Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Eyal GottliebThe laboratory for Metabolism in Health and Disease, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology Haifa, Israel.
Gil LeibowitzDiabetes Unit and Endocrine Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Hadassah Medical Center · ILInstitute of Cancer Research · CARappaport Family Institute for Research in the Medical Sciences · ILHebrew University of Jerusalem · ILUniversity of Miami · US

Funding

BLRD VA I01 BX002728
6 · The paper itself

Abstract

Diabetes is associated with increased risk for kidney disease, heart failure, and mortality. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) prevent these adverse outcomes; however, the mechanisms involved are not clear. We generated a roadmap of the metabolic alterations that occur in different organs in diabetes and in response to SGLT2i. In vivo metabolic labeling with 13C-glucose in normoglycemic and diabetic mice treated with or without dapagliflozin, followed by metabolomics and metabolic flux analyses, showed that, in diabetes, glycolysis and glucose oxidation are impaired in the kidney, liver, and heart. Treatment with dapagliflozin failed to rescue glycolysis. SGLT2 inhibition increased glucose oxidation in all organs; in the kidney, this was associated with modulation of the redox state. Diabetes was associated with altered methionine cycle metabolism, evident by decreased betaine and methionine levels, whereas treatment with SGLT2i increased hepatic betaine along with decreased homocysteine levels. mTORC1 activity was inhibited by SGLT2i along with stimulation of AMPK in both normoglycemic and diabetic animals, possibly explaining the protective effects against kidney, liver, and heart diseases. Collectively, our findings suggest that SGLT2i induces metabolic reprogramming orchestrated by AMPK-mTORC1 signaling with common and distinct effects in various tissues, with implications for diabetes and aging.

Indexed as

Diabetes Mellitus, ExperimentalSodium-Glucose Transporter 2 InhibitorsAMP-Activated Protein KinasesAnimalsBenzhydryl CompoundsBetaineGlucoseGlucosidesMethionineMiceSodiumSodium-Glucose Transporter 2AMP-Activated Protein KinasesBenzhydryl CompoundsBetainedapagliflozinGlucoseGlucosidesMethionineSodiumSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsDiabetesGlucose metabolismMetabolismSignal transductionTherapeutics

Identifiers

PMID36809274
PMCPMC10132155
OpenAlexW4321444920

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.