Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion

• Published in: Nature medicine Vol. 21; no. 5; pp. 512 - 517
• Main Authors: Bonner, Caroline, Kerr-Conte, Julie, Gmyr, Valéry, Queniat, Gurvan, Moerman, Ericka, Thévenet, Julien, Beaucamps, Cédric, Delalleau, Nathalie, Popescu, Iuliana, Malaisse, Willy J, Sener, Abdullah, Deprez, Benoit, Abderrahmani, Amar, Staels, Bart, Pattou, François
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01.05.2015; Nature Publishing Group
• Subjects: 14; 14/19; 38/1; 38/109; 38/39; 38/89; 692/699/2743/137/773; 82; Administration, Oral; Adult; Animals; Benzhydryl Compounds - chemistry; Biomedicine; Blood Glucose - chemistry; Cancer Research; Carrier proteins; Cell Separation; Dapagliflozin; Dosage and administration; Drug therapy; Female; Flow Cytometry; Gene Expression Profiling; Gene Expression Regulation; Gene Silencing; Glucagon; Glucagon - blood; Glucagon - metabolism; Glucagon-Secreting Cells - metabolism; Gluconeogenesis; Glucose; Glucosides - chemistry; Health aspects; Hepatocyte Nuclear Factor 4 - metabolism; Humans; Infectious Diseases; Insulin Resistance; letter; Male; Metabolic Diseases; Mice; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; Molecular Medicine; Neurosciences; Pancreas; RNA, Small Interfering - metabolism; Sodium-Glucose Transporter 1 - metabolism; Sodium-Glucose Transporter 2 - metabolism; Type 2 diabetes

The recently approved drug dapagliflozin is now shown to increase glucagon secretion by acting on pancreatic alpha cells, which has implications for the potency of its antidiabetic effects Type 2 diabetes (T2D) is characterized by chronic hyperglycemia resulting from a deficiency in insulin signalin...