Altered metabolic gene expression in the brain of a triprolyl-human amylin transgenic mouse model of type 2 diabetes.

ABSTRACT: Type 2 diabetes mellitus is a major health concern worldwide; however, the molecular mechanism underlying its development is poorly understood. The hormone amylin is postulated to be involved, as human amylin forms amyloid in the pancreases of diabetic patients, and oligomers have been shown to be cytotoxic to β-cells. As rodent amylin is non-amyloidogenic, mice expressing human amylin have been developed to investigate this hypothesis. However, it is not possible to differentiate the effects of amylin overexpression from β-cell loss in these models. We have developed transgenic mice that overexpress [^{25, 28, 29} triprolyl]human amylin, a non-amyloidogenic variant of amylin, designated the Line 44 model. This model allows us to investigate the effects of chronic overexpression of

SUBMITTER: Nie T 

PROVIDER: S-EPMC6787337 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature