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

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

Adenosine triphosphate-sensitive K+ (KATP) channels play an essential role in glucose-induced insulin secretion from pancreatic β-cells. It was recently reported that the KATP channel is also found in the enteroendocrine K-cells and L-cells that secrete glucose-dependent insulinotropic polypeptide (...

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Main Authors: Seino, Yusuke, Ogata, Hidetada, Maekawa, Ryuya, Izumoto, Takako, Iida, Atsushi, Harada, Norio, Miki, Takashi, Seino, Susumu, Inagaki, Nobuya, Tsunekawa, Shin, Oiso, Yutaka, Hamada, Yoji
Format: Online
Language:English
Published: John Wiley & Sons, Ltd 2015
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578490/
id pubmed-4578490
recordtype oai_dc
spelling pubmed-45784902015-09-28 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 Articles Adenosine triphosphate-sensitive K+ (KATP) channels play an essential role in glucose-induced insulin secretion from pancreatic β-cells. It was recently reported that the KATP 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 KATP channel in fructose-induced GIP, GLP-1 and insulin secretion in mice. Fructose stimulated GIP secretion, but pretreatment with diazoxide, a KATP 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 KATP 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 in Kir6.2+/+ mice and in MIN6-K8 β-cells. These results show that fructose-induced GIP and GLP-1 secretion is KATP channel-independent and that fructose-induced insulin secretion is KATP channel-dependent. John Wiley & Sons, Ltd 2015-09 2015-05-03 /pmc/articles/PMC4578490/ /pubmed/26417408 http://dx.doi.org/10.1111/jdi.12356 Text en © 2015 The Authors. Journal of Diabetes Investigation published by Asian Association of the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Seino, Yusuke
Ogata, Hidetada
Maekawa, Ryuya
Izumoto, Takako
Iida, Atsushi
Harada, Norio
Miki, Takashi
Seino, Susumu
Inagaki, Nobuya
Tsunekawa, Shin
Oiso, Yutaka
Hamada, Yoji
spellingShingle Seino, Yusuke
Ogata, Hidetada
Maekawa, Ryuya
Izumoto, Takako
Iida, Atsushi
Harada, Norio
Miki, Takashi
Seino, Susumu
Inagaki, Nobuya
Tsunekawa, Shin
Oiso, Yutaka
Hamada, Yoji
Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
author_facet Seino, Yusuke
Ogata, Hidetada
Maekawa, Ryuya
Izumoto, Takako
Iida, Atsushi
Harada, Norio
Miki, Takashi
Seino, Susumu
Inagaki, Nobuya
Tsunekawa, Shin
Oiso, Yutaka
Hamada, Yoji
author_sort Seino, Yusuke
title Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
title_short Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
title_full Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
title_fullStr Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
title_full_unstemmed Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: Role of adenosine triphosphate-sensitive K+ channels
title_sort fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion: role of adenosine triphosphate-sensitive k+ channels
description Adenosine triphosphate-sensitive K+ (KATP) channels play an essential role in glucose-induced insulin secretion from pancreatic β-cells. It was recently reported that the KATP 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 KATP channel in fructose-induced GIP, GLP-1 and insulin secretion in mice. Fructose stimulated GIP secretion, but pretreatment with diazoxide, a KATP 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 KATP 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 in Kir6.2+/+ mice and in MIN6-K8 β-cells. These results show that fructose-induced GIP and GLP-1 secretion is KATP channel-independent and that fructose-induced insulin secretion is KATP channel-dependent.
publisher John Wiley & Sons, Ltd
publishDate 2015
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578490/
_version_ 1613478224844554240

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