Evidence mapPaperPMID 32896668Full record

ArticleMolecular metabolism2020

SGLT2 is not expressed in pancreatic α- and β-cells, and its inhibition does not directly affect glucagon and insulin secretion in rodents and humans.

Heeyoung Chae, Robert Augustin, Eva Gatineau, Eric Mayoux, Mohammed Bensellam, Nancy Antoine, Firas Khattab, Bao-Khanh Lai, Davide Brusa, Birgit Stierstorfer and 13 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
3.5field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  15. Dehydration-induced AVP stimulates glucagon release and ketogenesis.American journal of physiology. Endocrinology and metabolism · 2025
    Article
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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

23 authors at 8 institutions in 6 countries.

Heeyoung ChaePole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Robert AugustinDepartment of Cardiometabolic Disease Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Eva GatineauPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Eric MayouxDepartment of Cardiometabolic Disease Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Mohammed BensellamPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Nancy AntoinePole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Firas KhattabPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Bao-Khanh LaiPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Davide BrusaFlow Cytometry Platform, Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Birgit StierstorferDrug Discovery Sciences, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Holger KleinGlobal Computational Biology and Data Sciences, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Bilal SinghPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Lucie RuizPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium.
Michael PieperDepartment of Cardiometabolic Disease Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Michael MarkDepartment of Cardiometabolic Disease Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Pedro L HerreraDepartment of Genetic Medicine and Development, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Fiona M GribbleWellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK.
Frank ReimannWellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK.
Anne WojtusciszynLaboratory of Cellular Therapy for Diabetes, University Hospital of Montpellier, Montpellier, France; Department of Endocrinology, Diabetes and Metabolism, Lausanne University Hospital, Lausanne, Switzerland.
Christophe BrocaLaboratory of Cellular Therapy for Diabetes, University Hospital of Montpellier, Montpellier, France.
Nano RitaSan Raffaele Diabetes Research Institute, IRCCS Ospedale San Raffaele, 20132, Milan, Italy.
Lorenzo PiemontiSan Raffaele Diabetes Research Institute, IRCCS Ospedale San Raffaele, 20132, Milan, Italy; Università Vita-Salute San Raffaele, Milan, Italy.
Patrick GilonPole of Endocrinology, Diabetes, and Nutrition (EDIN), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain (UCLouvain), 1200, Brussels, Belgium. Electronic address: patrick.gilon@uclouvain.be.
UCLouvain · BEBoehringer Ingelheim (Germany) · DEWellcome/MRC Institute of Metabolic Science · GBCentre Hospitalier Universitaire de Montpellier · FRIRCCS Ospedale San Raffaele · ITUniversity Hospital of Lausanne · CHUniversity of Geneva · CHVita-Salute San Raffaele University · IT

Funding

Medical Research Council MC_UU_00014/3Medical Research Council MC_UU_12012/3NIDDK NIH HHS UC4 DK098085Wellcome Trust 106262/Z/14/ZWellcome Trust 106263/Z/14/Z
6 · The paper itself

Abstract

objectiveSodium-glucose cotransporter 2 (SGLT2) inhibitors (SGLT2i), or gliflozins, are anti-diabetic drugs that lower glycemia by promoting glucosuria, but they also stimulate endogenous glucose and ketone body production. The likely causes of these metabolic responses are increased blood glucagon levels, and decreased blood insulin levels, but the mechanisms involved are hotly debated. This study verified whether or not SGLT2i affect glucagon and insulin secretion by a direct action on islet cells in three species, using multiple approaches.

methodsWe tested the in vivo effects of two selective SGLT2i (dapagliflozin, empagliflozin) and a SGLT1/2i (sotagliflozin) on various biological parameters (glucosuria, glycemia, glucagonemia, insulinemia) in mice. mRNA expression of SGLT2 and other glucose transporters was assessed in rat, mouse, and human FACS-purified α- and β-cells, and by analysis of two human islet cell transcriptomic datasets. Immunodetection of SGLT2 in pancreatic tissues was performed with a validated antibody. The effects of dapagliflozin, empagliflozin, and sotagliflozin on glucagon and insulin secretion were assessed using isolated rat, mouse and human islets and the in situ perfused mouse pancreas. Finally, we tested the long-term effect of SGLT2i on glucagon gene expression.

resultsSGLT2 inhibition in mice increased the plasma glucagon/insulin ratio in the fasted state, an effect correlated with a decline in glycemia. Gene expression analyses and immunodetections showed no SGLT2 mRNA or protein expression in rodent and human islet cells, but moderate SGLT1 mRNA expression in human α-cells. However, functional experiments on rat, mouse, and human (29 donors) islets and the in situ perfused mouse pancreas did not identify any direct effect of dapagliflozin, empagliflozin or sotagliflozin on glucagon and insulin secretion. SGLT2i did not affect glucagon gene expression in rat and human islets.

conclusionsThe data indicate that the SGLT2i-induced increase of the plasma glucagon/insulin ratio in vivo does not result from a direct action of the gliflozins on islet cells.

Indexed as

AnimalsBenzhydryl CompoundsBlood GlucoseGlucagonGlucagon-Like Peptide 1Glucagon-Secreting CellsGlucoseGlucosidesHumansInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMicePancreasRatsBenzhydryl CompoundsBlood GlucosedapagliflozinGlucagonGlucagon-Like Peptide 1GlucoseGlucosidesInsulinSLC5A2 protein, humanSlc5a2 protein, mouseSlc5a2 protein, ratSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsDiabetesGliflozinsGlucagonInsulinSGLT2 inhibitor

Identifiers

PMID32896668
PMCPMC7554656
OpenAlexW3084101089

What Socratic holds

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LicenceCC BY-NC-ND
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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.