Higashi Shintaro, Katagi Kazuhiko, Shintani Norihito, Ikeda Kazuya, Sugimoto Yukihiko, Tsuchiya Soken, Inoue Naoki, Tanaka Shota, Koumoto Mai, Kasai Atsushi, Nakazawa Takanobu, Hayata-Takano Atsuko, Hamagami Ken-Ichi, Tomimoto Shuhei, Yoshida Takuya, Ohkubo Tadayasu, Nagayasu Kazuki, Ago Yukio, Onaka Yusuke, Hashimoto Ryota, Ichikawa Atsushi, Baba Akemichi, Hashimoto Hitoshi
Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan; Research Fellow of the Japan Society for the Promotion of Science, Japan.
Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan.
Biochem Biophys Res Commun. 2015 Jun 12;461(4):612-7. doi: 10.1016/j.bbrc.2015.04.074. Epub 2015 Apr 23.
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.
我们通过构建在胰腺β细胞中过表达p13(p13-Tg)的转基因小鼠,研究了由1110001J03Rik编码的p13的胰腺功能,该基因在高脂喂养的糖尿病小鼠胰岛中的表达降低。p13-Tg小鼠表现出正常的基础葡萄糖代谢;然而,在高脂喂养条件下,这些动物的葡萄糖诱导的第一相和总胰岛素分泌增加,葡萄糖处置改善,胰岛面积增大,有丝分裂胰岛素阳性细胞增多。此外,高脂饮食诱导的4-羟基壬烯醛免疫反应性(脂质过氧化应激的可靠标志物和致病因子)在p13-Tg小鼠胰岛中显著降低。这些结果表明,p13是一种新型胰腺因子,对2型糖尿病具有多种有益作用。