GLUCOSE HOMEOSTASIS, INSULIN SECRETION, AND ISLET PHOSPHOLIPIDS IN MICE

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 对转基因胰岛素瘤细胞的研究表明，通过磷脂酶A(2)(iPLA(2)β)的组参与放大葡萄糖诱导的胰岛素分泌。例如，过表达iPLA(2)β的INS-1胰岛素瘤细胞对葡萄糖和cAMP提高剂表现出放大的胰岛素分泌反应。为了确定在整个动物中是否发生类似的效应，我们制备了转基因(TG)小鼠，在其中大鼠胰岛素1启动子(RIP)驱动iPLA2(2)β的过表达，并且两个特征的TG小鼠品系表现出相似的表型。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Studies with genetically modified insulinoma cells suggest that group VIA phospholipase A(2) (iPLA(2)beta) participates in amplifying glucose-induced insulin secretion. INS-1 insulinoma cells that overexpress iPLA(2)beta, for example, exhibit amplified insulin-secretory responses to glucose and cAMP-elevating agents. To determine whether similar effects occur in whole animals, we prepared transgenic (TG) mice in which the rat insulin 1 promoter (RIP) drives iPLA(2)beta overexpression, and two characterized TG mouse lines exhibit similar phenotypes.