| Literature DB >> 25912136 |
Shintaro Higashi1, Kazuhiko Katagi2, Norihito Shintani3, Kazuya Ikeda1, Yukihiko Sugimoto4, Soken Tsuchiya4, Naoki Inoue2, Shota Tanaka2, Mai Koumoto2, Atsushi Kasai2, Takanobu Nakazawa5, Atsuko Hayata-Takano6, Ken-Ichi Hamagami2, Shuhei Tomimoto2, Takuya Yoshida7, Tadayasu Ohkubo7, Kazuki Nagayasu5, Yukio Ago8, Yusuke Onaka9, Ryota Hashimoto10, Atsushi Ichikawa11, Akemichi Baba12, Hitoshi Hashimoto13.
Abstract
We examined the pancreatic function of p13 encoded by 1110001J03Rik, whose expression is decreased in pancreatic islets in high-fat-fed diabetic mice, by generating transgenic mice overexpressing p13 (p13-Tg) in pancreatic β-cells. p13-Tg mice showed normal basal glucose metabolism; however, under high-fat feeding, these animals showed augmented glucose-induced first-phase and total insulin secretion, improved glucose disposal, greater islet area and increased mitotic insulin-positive cells. In addition, high-fat diet-induced 4-hydroxynonenal immunoreactivity, a reliable marker and causative agent of lipid peroxidative stress, was significantly decreased in p13-Tg mouse islets. These results indicate that p13 is a novel pancreatic factor exerting multiple beneficial effects against type 2 diabetes.Entities:
Keywords: 1110001J03Rik; Glucose-induced insulin secretion; High-fat diet; Lipid peroxidative stress; PACAP; Type 2 diabetes
Mesh：
Year: 2015 PMID： 25912136 DOI： 10.1016/j.bbrc.2015.04.074
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575