TY - JOUR
T1 - Fructose induces glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and insulin secretion
T2 - Role of adenosine triphosphate-sensitive K+ channels
AU - Seino, Yusuke
AU - Ogata, Hidetada
AU - Maekawa, Ryuya
AU - Izumoto, Takako
AU - Iida, Atsushi
AU - Harada, Norio
AU - Miki, Takashi
AU - Seino, Susumu
AU - Inagaki, Nobuya
AU - Tsunekawa, Shin
AU - Oiso, Yutaka
AU - Hamada, Yoji
N1 - Publisher Copyright:
© 2015 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd.
PY - 2015/9/1
Y1 - 2015/9/1
N2 - 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. Fructose significantly stimulated insulin secretion in Kir6.2+/+ mice but not in mice lacking KATP channels (Kir6.2-/-).
AB - 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. Fructose significantly stimulated insulin secretion in Kir6.2+/+ mice but not in mice lacking KATP channels (Kir6.2-/-).
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U2 - 10.1111/jdi.12356
DO - 10.1111/jdi.12356
M3 - Article
AN - SCOPUS:84940609646
SN - 2040-1116
VL - 6
SP - 522
EP - 526
JO - Journal of Diabetes Investigation
JF - Journal of Diabetes Investigation
IS - 5
ER -
