Cell metabolism · 2014
The role of β cell glucagon-like peptide-1 signaling in glucose regulation and response to diabetes drugs.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Smith Eric P, An Zhibo, Wagner Constance, Lewis Alfor G, Cohen Eric B, Li Bailing, Mahbod Parinaz, Sandoval Darleen, Perez-Tilve Diego, Tamarina Natalia, Philipson Louis H, Stoffers Doris A, Seeley Randy J, D'Alessio David A
Аннотация
Glucagon-like peptide-1 (GLP-1), an insulinotropic gut peptide released after eating, is essential for normal glucose tolerance (GT). To determine whether this effect is mediated directly by GLP-1 receptors (GLP1R) on islet β cells, we developed mice with β cell-specific knockdown of Glp1r. β cell Glp1r knockdown mice had impaired GT after intraperitoneal (i.p.) glucose and did not secrete insulin in response to i.p. or intravenous GLP-1. However, they had normal GT after oral glucose, a response that was impaired by a GLP1R antagonist. β cell Glp1r knockdown mice had blunted responses to a GLP1R agonist but intact glucose lowering with a dipeptidylpeptidase 4 (DPP-4) inhibitor. Thus, in mice, β cell Glp1rs are required to respond to hyperglycemia and exogenous GLP-1, but other factors compensate for reduced GLP-1 action during meals. These results support a role for extraislet GLP1R in oral glucose tolerance and paracrine regulation of β cells by islet GLP-1.