No direct effect of SGLT2 activity on glucagon secretion.


Journal

Diabetologia
ISSN: 1432-0428
Titre abrégé: Diabetologia
Pays: Germany
ID NLM: 0006777

Informations de publication

Date de publication:
06 2019
Historique:
received: 17 11 2018
accepted: 12 02 2019
pubmed: 25 3 2019
medline: 14 1 2020
entrez: 24 3 2019
Statut: ppublish

Résumé

Sodium-glucose cotransporter (SGLT) 2 inhibitors constitute a new class of glucose-lowering drugs, but they increase glucagon secretion, which may counteract their glucose-lowering effect. Previous studies using static incubation of isolated human islets or the glucagon-secreting cell line α-TC1 suggested that this results from direct inhibition of alpha cell SGLT1/2-activity. The aim of this study was to test whether the effects of SGLT2 on glucagon secretion demonstrated in vitro could be reproduced in a more physiological setting. We explored the effect of SGLT2 activity on glucagon secretion using isolated perfused rat pancreas, a physiological model for glucagon secretion. Furthermore, we investigated Slc5a2 (the gene encoding SGLT2) expression in rat islets as well as in mouse and human islets and in mouse and human alpha, beta and delta cells to test for potential inter-species variations. SGLT2 protein content was also investigated in mouse, rat and human islets. Glucagon output decreased three- to fivefold within minutes of shifting from low (3.5 mmol/l) to high (10 mmol/l) glucose (4.0 ± 0.5 pmol/15 min vs 1.3 ± 0.3 pmol/15 min, p < 0.05). The output was unaffected by inhibition of SGLT1/2 with dapagliflozin or phloridzin or by addition of the SGLT1/2 substrate α-methylglucopyranoside, whether at low or high glucose concentrations (p = 0.29-0.99). Insulin and somatostatin secretion (potential paracrine regulators) was also unaffected. Slc5a2 expression and SGLT2 protein were marginal or below detection limit in rat, mouse and human islets and in mouse and human alpha, beta and delta cells. Our combined data show that increased plasma glucagon during SGLT2 inhibitor treatment is unlikely to result from direct inhibition of SGLT2 in alpha cells, but instead may occur downstream of their blood glucose-lowering effects.

Identifiants

pubmed: 30903205
doi: 10.1007/s00125-019-4849-6
pii: 10.1007/s00125-019-4849-6
pmc: PMC7212061
mid: EMS86318
doi:

Substances chimiques

Insulin 0
Sodium-Glucose Transporter 1 0
Sodium-Glucose Transporter 2 0
Somatostatin 51110-01-1
Glucagon 9007-92-5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1011-1023

Subventions

Organisme : Wellcome Trust
ID : 106262
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 106263/Z/14/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 106262/Z/14/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 106263
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/3
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00014/3
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Medical Research Council
ID : MRC_MC_UU_12012/3
Pays : United Kingdom

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Auteurs

Rune E Kuhre (RE)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.
Novo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Seyed M Ghiasi (SM)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.
Department of Biology, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.

Alice E Adriaenssens (AE)

Metabolic Research Laboratories and Medical Research Council Metabolic Diseases Unit, Wellcome Trust-Medical Research Council, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.

Nicolai J Wewer Albrechtsen (NJ)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.
Novo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.

Daniel B Andersen (DB)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.
Novo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Alexander Aivazidis (A)

Translational Science, Cardiovascular, Renal and Metabolism, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.

Lihua Chen (L)

Translational Science, Cardiovascular, Renal and Metabolism, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.

Thomas Mandrup-Poulsen (T)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.

Cathrine Ørskov (C)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark.

Fiona M Gribble (FM)

Metabolic Research Laboratories and Medical Research Council Metabolic Diseases Unit, Wellcome Trust-Medical Research Council, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.

Frank Reimann (F)

Metabolic Research Laboratories and Medical Research Council Metabolic Diseases Unit, Wellcome Trust-Medical Research Council, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.

Nils Wierup (N)

Department of Experimental Medical Science, Faculty of Medicine, Lund University Diabetes Centre, Lund, Sweden.

Björn Tyrberg (B)

Translational Science, Cardiovascular, Renal and Metabolism, IMED Biotech Unit, AstraZeneca, Gothenburg, Sweden.

Jens J Holst (JJ)

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Blegdamsvej 3B, DK-2200, Copenhagen N, Denmark. jjholst@sund.ku.dk.
Novo Nordisk Foundation Centre for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. jjholst@sund.ku.dk.

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