SGLT1 in pancreatic α cells regulates glucagon secretion in mice, possibly explaining the distinct effects of SGLT2 inhibitors on plasma glucagon levels.


Journal

Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730

Informations de publication

Date de publication:
01 2019
Historique:
received: 20 09 2018
revised: 19 10 2018
accepted: 23 10 2018
pubmed: 13 11 2018
medline: 7 1 2020
entrez: 13 11 2018
Statut: ppublish

Résumé

It is controversial whether sodium glucose transporter (SGLT) 2 inhibitors increase glucagon secretion via direct inhibition of SGLT2 in pancreatic α cells. The role of SGLT1 in α cells is also unclear. We aimed to elucidate these points that are important not only for basic research but also for clinical insight. Plasma glucagon levels were assessed in the high-fat, high-sucrose diet (HFHSD) fed C57BL/6J mice treated with dapagliflozin or canagliflozin. RT-PCR, RNA sequence, and immunohistochemistry were conducted to test the expression of SGLT1 and SGLT2 in α cells. We also used αTC1 cells and mouse islets to investigate the molecular mechanism by which SGLT1 modulates glucagon secretion. Dapagliflozin, but not canagliflozin, increased plasma glucagon levels in HFHSD fed mice. SGLT1 and glucose transporter 1 (GLUT1), but not SGLT2, were expressed in αTC1 cells, mouse islets and human islets. A glucose clamp study revealed that the plasma glucagon increase associated with dapagliflozin could be explained as a response to acute declines in blood glucose. Canagliflozin suppressed glucagon secretion by inhibiting SGLT1 in α cells; consequently, plasma glucagon did not increase with canagliflozin, even though blood glucose declined. SGLT1 effect on glucagon secretion depended on glucose transport, but not glucose metabolism. Islets from HFHSD and db/db mice displayed higher SGLT1 mRNA levels and lower GLUT1 mRNA levels than the islets from control mice. These expression levels were associated with higher glucagon secretion. Furthermore, SGLT1 inhibitor and siRNA against SGLT1 suppressed glucagon secretion in isolated islets. These data suggested that a novel mechanism regulated glucagon secretion through SGLT1 in α cells. This finding possibly explained the distinct effects of dapagliflozin and canagliflozin on plasma glucagon levels in mice.

Identifiants

pubmed: 30416006
pii: S2212-8778(18)30937-2
doi: 10.1016/j.molmet.2018.10.009
pmc: PMC6323192
pii:
doi:

Substances chimiques

Benzhydryl Compounds 0
Blood Glucose 0
Glucosides 0
Hypoglycemic Agents 0
Insulin 0
Slc5a1 protein, mouse 0
Slc5a2 protein, mouse 0
Sodium-Glucose Transporter 1 0
Sodium-Glucose Transporter 2 0
Sodium-Glucose Transporter 2 Inhibitors 0
Canagliflozin 0SAC974Z85
dapagliflozin 1ULL0QJ8UC
Gastric Inhibitory Polypeptide 59392-49-3
Glucagon-Like Peptide 1 89750-14-1
Glucagon 9007-92-5
Glucose IY9XDZ35W2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-12

Informations de copyright

Copyright © 2018 The Authors. Published by Elsevier GmbH.. All rights reserved.

Références

J Clin Invest. 2012 Jan;122(1):4-12
pubmed: 22214853
N Engl J Med. 2015 Sep 3;373(10):974-6
pubmed: 26332554
Nat Med. 2015 May;21(5):512-7
pubmed: 25894829
Diabetes Care. 2010 Oct;33(10):2217-24
pubmed: 20566676
Diabetes. 2011 Mar;60(3):890-8
pubmed: 21357472
Diabetologia. 2008 Dec;51(12):2263-70
pubmed: 18795252
Sci Rep. 2016 Aug 18;6:31214
pubmed: 27535321
Nat Rev Endocrinol. 2015 Jun;11(6):329-38
pubmed: 25850661
Mol Endocrinol. 2010 Aug;24(8):1605-14
pubmed: 20592160
Diabetes. 1977 May;26(5):445-52
pubmed: 856648
Biochem Biophys Res Commun. 2017 Oct 14;492(2):161-165
pubmed: 28803984
Trends Endocrinol Metab. 2015 Jul;26(7):337-8
pubmed: 26059706
Diabetes Obes Metab. 2013 Apr;15(4):372-82
pubmed: 23279307
Int J Cancer. 1982 Jul 15;30(1):65-7
pubmed: 7118298
Endocr J. 2015;62(12):1133-7
pubmed: 26522271
J Clin Endocrinol Metab. 2000 Nov;85(11):4053-9
pubmed: 11095432
Ann Surg. 1998 Mar;227(3):390-7
pubmed: 9527062
Diabetes. 2012 Jan;61(1):187-96
pubmed: 22124465
Diabetes. 2015 Oct;64(10):3564-72
pubmed: 26130763
Mol Aspects Med. 2013 Apr-Jun;34(2-3):183-96
pubmed: 23506865
Diabetes Metab. 2017 Dec;43(6):512-520
pubmed: 28499695
Diabetes Obes Metab. 2017 Jun;19(6):874-882
pubmed: 28177187
Mol Cell Biol. 2001 Aug;21(16):5624-30
pubmed: 11463843
J Clin Invest. 2014 Feb;124(2):499-508
pubmed: 24463454
Diabetes. 2003 May;52(5):1147-54
pubmed: 12716745
Diabetologia. 2007 Feb;50(2):370-9
pubmed: 17136393
Eur J Endocrinol. 2014 Mar 08;170(4):529-38
pubmed: 24412928
Cell Metab. 2010 Jun 9;11(6):543-553
pubmed: 20519125
Diabetes Care. 2013 Aug;36(8):2154-61
pubmed: 23412078
Diabetes. 2005 Jun;54(6):1789-97
pubmed: 15919801
Am J Surg. 1985 Dec;150(6):676-9
pubmed: 4073359
J Clin Pharmacol. 2013 Jun;53(6):601-10
pubmed: 23670707
Diabetes Care. 2012 Jun;35(6):1232-8
pubmed: 22492586
J Intern Med. 2016 May;279(5):485-93
pubmed: 26728692
J Biol Chem. 1995 Apr 14;270(15):8971-5
pubmed: 7721807
J Clin Invest. 2014 Feb;124(2):509-14
pubmed: 24463448
Am J Physiol Endocrinol Metab. 2014 Jun 1;306(11):E1225-38
pubmed: 24714398
Lancet. 2010 Jun 26;375(9733):2223-33
pubmed: 20609968
Pharmacol Res. 2017 Apr;118:71-81
pubmed: 27389050
Diabetologia. 2012 Sep;55(9):2445-55
pubmed: 22638549
Mol Metab. 2018 Jul;13:67-76
pubmed: 29859847
Diabetes Obes Metab. 2011 Apr;13(4):357-65
pubmed: 21226818
J Biol Chem. 2010 May 7;285(19):14389-98
pubmed: 20231269
Diabetes. 2017 Aug;66(8):2144-2149
pubmed: 28385801
Front Neurosci. 2016 Nov 08;10:502
pubmed: 27877104
Cell Metab. 2016 Oct 11;24(4):593-607
pubmed: 27667667
Diabetes. 1987 Mar;36(3):274-83
pubmed: 2879757
Anal Bioanal Chem. 2017 Oct;409(25):5911-5918
pubmed: 28801845
Diabetes. 2015 Feb;64(2):370-82
pubmed: 25157092
Proc Natl Acad Sci U S A. 2015 Jul 28;112(30):E4111-9
pubmed: 26170283
Hepatol Res. 2017 Mar;47(4):266-280
pubmed: 28019064

Auteurs

Takayoshi Suga (T)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan; Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Osamu Kikuchi (O)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Masaki Kobayashi (M)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Sho Matsui (S)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Hiromi Yokota-Hashimoto (H)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Eri Wada (E)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Daisuke Kohno (D)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Tsutomu Sasaki (T)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.

Kazusane Takeuchi (K)

Cosmic Corporation Co., Ltd., Bunkyo-ku, Tokyo, Japan.

Satoru Kakizaki (S)

Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Masanobu Yamada (M)

Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Tadahiro Kitamura (T)

Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan. Electronic address: kitamura@gunma-u.ac.jp.

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Classifications MeSH