@article{472dcc20ab5011ddb5e9000ea68e967b,
title = "Distinct effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 on insulin secretion and gut motility.",
abstract = "Glucose-induced insulin secretion from pancreatic beta-cells depends critically on ATP-sensitive K(+) channel (K(ATP) channel) activity, but it is not known whether K(ATP) channels are involved in the potentiation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP). In mice lacking K(ATP) channels (Kir6.2(-/-) mice), we found that pretreatment with GIP in vivo failed to blunt the rise in blood glucose levels after oral glucose load. In Kir6.2(-/-) mice, potentiation of insulin secretion by GIP in vivo was markedly attenuated, indicating that K(ATP) channels are essential in the insulinotropic effect of GIP. In contrast, pretreatment with glucagon-like peptide-1 (GLP-1) in Kir6.2(-/-) mice potentiated insulin secretion and blunted the rise in blood glucose levels. We also found that GLP-1 inhibited gut motility whereas GIP did not. Perfusion experiments of Kir6.2(-/-) mice revealed severely impaired potentiation of insulin secretion by 1 nmol/l GIP and substantial potentiation by 1 nmol/l GLP-1. Although both GIP and GLP-1 increase the intracellular cAMP concentration and potentiate insulin secretion, these results demonstrate that the GLP-1 and GIP signaling pathways involve the K(ATP) channel differently.",
author = "Takashi Miki and Kohtaro Minami and Hidehiro Shinozaki and Kimio Matsumura and Atsunori Saraya and Hiroki Ikeda and Yuichiro Yamada and Holst, {Jens Juul} and Susumu Seino",
note = "Keywords: Animals; Arginine; Blood Glucose; Food; Gastric Inhibitory Polypeptide; Gastrointestinal Motility; Glucagon; Glucagon-Like Peptide 1; Insulin; Islets of Langerhans; Mice; Mice, Knockout; Pancreas; Peptide Fragments; Potassium Channels; Potassium Channels, Inwardly Rectifying; Protein Precursors; Time Factors",
year = "2005",
language = "English",
volume = "54",
pages = "1056--63",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "4",
}