GLUCOSE HOMEOSTASIS, INSULIN SECRETION, AND ISLET PHOSPHOLIPIDS IN MICE

小鼠的葡萄糖稳态、胰岛素分泌和胰岛磷脂

• 批准号: 7953994
• 负责人: S BAO
• 金额: $ 0.58万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7953994
• 关键词: A Mouse; Animals; Cells; Computer Retrieval of Information on Scientific Projects Database; Cyclic AMP; Exhibits; Funding; Glucose; Grant; Institution; Insulin; Mass Spectrum Analysis; Phenotype; Phospholipases A; Phospholipids; Rattus; Research; Research Personnel; Resources; Source; Transgenic Mice; United States National Institutes of Health; biomedical resource; blood glucose regulation; human PLA2G6 protein; insulin secretion; insulinoma; islet; overexpression; promoter; response

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.

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