p13 overexpression in pancreatic b-cells ameliorates type 2 diabetes in high-fat-fed mice
p13 overexpression in pancreatic b-cells ameliorates type 2 diabetes in high-fat-fed mice
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胰腺 B 细胞中 p13 过度表达可改善高脂喂养小鼠的 2 型糖尿病
DOI：
10.1016/j.bbrc.2015.04.074
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发表时间：
2015
影响因子：
3.1
通讯作者：
S. et al.
中科院分区：
文献类型：
--
作者：
Higashi;S. et al.
我们通过在胰腺β细胞中产生过表达p13（p13-Tg）的转基因小鼠来检测由1110001 J 03 Rik编码的p13的胰腺功能，其在高脂喂养的糖尿病小鼠的胰岛中的表达降低。p13-Tg小鼠显示正常的基础葡萄糖代谢;然而，在高脂肪喂养下，这些动物显示葡萄糖诱导的第一时相和总胰岛素分泌增加，葡萄糖处理改善，胰岛面积增大，有丝分裂胰岛素阳性细胞增加。此外，高脂饮食诱导的4-羟基壬烯醛免疫反应，一个可靠的标志物和脂质过氧化应激的病原体，在p13-Tg小鼠胰岛显着下降。这些结果表明，p13是一种新的胰腺因子，对2型糖尿病发挥多种有益作用。
We examined the pancreatic function of p13 encoded by1110001J03Rik, 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.