Journal Article Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K[+] channels

Seino, Yusuke  ,  Ogata, Hidetada  ,  Maekawa, Ryuya  ,  Izumoto, Takako  ,  Iida, Atsushi  ,  Harada, Norio  ,  Miki, Takashi  ,  Seino, Susumu  ,  Inagaki, Nobuya  ,  Tsunekawa, Shin  ,  Oiso, Yutaka  ,  Hamada, Yoji

6 ( 5 )  , pp.522 - 526 , 2015-09 , Asian Association of the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd
Adenosine triphosphate-sensitive K[+] (K[ATP]) channels play an essential role in glucose-induced insulin secretion from pancreatic β-cells. It was recently reported that the K[ATP] channel is also found in the enteroendocrine K-cells and L-cells that secrete glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), respectively. In the present study, we investigated the involvement of the K[ATP] channel in fructose-induced GIP, GLP-1 and insulin secretion in mice. Fructose stimulated GIP secretion, but pretreatment with diazoxide, a K[ATP] channel activator, did not affect fructose-induced GIP secretion under streptozotocin-induced hyperglycemic conditions. Fructose significantly stimulated insulin secretion in Kir6.2[+/+] mice, but not in mice lacking K[ATP] channels (Kir6.2[−/−]), and fructose stimulated GLP-1 secretion in both Kir6.2[+/+]mice and Kir6.2[−/−] mice under the normoglycemic condition. In addition, diazoxide completely blocked fructose-induced insulin secretion inKir6.2[+/+] mice and in MIN6-K8 β-cells. These results show that fructose-induced GIP and GLP-1 secretion is K[ATP] channel-independent and that fructose-induced insulin secretion is K[ATP] channel-dependent.

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