| Literature DB >> 31390560 |
Chiara Saponaro1, Valéry Gmyr1, Julien Thévenet1, Ericka Moerman1, Nathalie Delalleau1, Gianni Pasquetti1, Anais Coddeville1, Audrey Quenon1, Mehdi Daoudi1, Thomas Hubert1, Marie-Christine Vantyghem2, Corinne Bousquet3, Yvan Martineau3, Julie Kerr-Conte1, Bart Staels4, François Pattou5, Caroline Bonner6.
Abstract
The newest classes of anti-diabetic agents include sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 receptor (GLP1R) agonists. The SGLT2 inhibitor dapagliflozin reduces glucotoxicity by glycosuria but elevates glucagon secretion. The GLP1R agonist liraglutide inhibits glucagon; therefore, we hypothesize that the cotreatment of dapagliflozin with liraglutide could reduce hyperglucagonemia and hyperglycemia. Here we use five complementary models: human islet cultures, healthy mice, db/db mice, diet-induced obese (DIO) mice, and somatostatin receptor-2 (SSTR2) KO mice. A single administration of liraglutide and dapagliflozin in combination improves glycemia and reduces dapagliflozin-induced glucagon secretion in diabetic mice. Chronic treatment with liraglutide and dapagliflozin produces a sustainable reduction of glycemia compared with each drug alone. Moreover, liraglutide reduces dapagliflozin-induced glucagon secretion by enhancing somatostatin release, as demonstrated by SSTR2 inhibition in human islets and in mice. Collectively, these data provide mechanistic insights into how intra-islet GLP1R activation is critical for the regulation of glucose homeostasis.Entities:
Keywords: GLP1R; dapagliflozin; glucagon; insulin; liraglutide; somatostatin; type 2 diabetes
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Year: 2019 PMID: 31390560 DOI: 10.1016/j.celrep.2019.07.009
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423