Modification of diabetic phenotype by Alzheimer's disease

我们先前表明，阿尔茨海默氏病（AD）在小鼠中表现为糖尿病表型。为了探索这一机制，我们开始创建APP Tet-off小鼠。血浆A β可能介导外周胰岛素抵抗。我们发现在AD模型中，葡萄糖负荷后血浆Abeta水平升高。在人类中，虽然变化幅度远小于AD转基因小鼠，但AD和非AD患者口服葡萄糖负荷后血浆Abeta水平的变化不同。这些数据表明，AD使糖尿病表型恶化的可能机制之一可能归因于血浆Abeta。我们现在正在构建APP Tet-off质粒，并将创建APP tet-off小鼠以控制APP表达和暴露于糖尿病的时间。

We previously showed that Alzheimer's disease (AD) aggravates the diabetic phenotype in mice. To explore this mechanism, we initiated to create APP Tet-off mice. Plasma Abeta may mediate peripheral insulin resistance. We found plasma Abeta level is increased after glucose loading in an AD model. In humans, although the magnitude of changes is much smaller than in AD transgenic mice, the changes in plasma Abeta levels after oral glucose loading are different between AD and non-AD patients. These data suggest that one of the possible mechanisms by which AD aggravates the diabetic phenotype might be attributable to plasma Abeta. We are now constructing APP Tet-off plasmid and will create APP tet-off mice to control the periods of APP expression and exposure to diabetes.