USE OF AN IN VIVO MODEL SYSTEM TO INVESTIGATE NIDDM

使用体内模型系统研究 NIDDM

• 批准号: 3745453
• 负责人: J EGAN
• 金额: --
• 依托单位: NATIONAL INSTITUTE ON AGING
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3745453
• 关键词: aging; disease /disorder model; disease /disorder proneness /risk; glucagon; glucokinase; hormone regulation /control mechanism; insulin; laboratory rat; messenger RNA; noninsulin dependent diabetes mellitus; pancreatic islet function; secretion

Age is an independent risk factor for NIDDM. A decline in insulin secretion and a decrease in insulin action occur as people age. This combination makes people more prone to develop NIDDM. A similar phenomenon occurs in Wistar rats. We are using the beta cells from Wistar rats in the aged colony at the GRC to study changes with insulin secretion. We found that mRNA for insulin is preferentially diminished in islets, with glucokinase and glucagon messages unaffected. Therefore, one can envision when a stress is put on the system so more insulin is required, diabetes could result. We are exploring what factors lead to this diminution of insulin message and the possibility that we can prevent or reverse it. We have found the GLP-1 can somewhat restore the number of cells that are again responsive.

年龄是NIDDM的独立危险因素。 胰岛素下降 随着人们年龄的增长，胰岛素分泌和胰岛素作用的减少发生。 这 联合使用会使人们更容易患上NIDDM。 类似的 这种现象发生在Wistar大鼠身上。 我们用的是 老年群体中的Wistar大鼠在GRC研究胰岛素的变化 分泌物 我们发现，胰岛素mRNA的优先减少， 胰岛，葡萄糖激酶和胰高血糖素信息不受影响。 因此，我们认为， 我们可以想象当系统受到压力时， 如果需要，可能会导致糖尿病。 我们正在探讨是什么因素导致 这种胰岛素信息的减少以及我们可以 我们已经发现GLP-1可以在一定程度上恢复 有反应的细胞数量。