NIH Reporter #5R01DK138471-03

Loss of insulin signaling across functional pancreas compartments as a major pathogenic mechanism underlying diabetic exocrine pancreatopathy

Research project funded by NIDDK to study the role of insulin signaling in pancreas compartments and its impact on type 1 diabetes progression, focusing on exocrine tissue, microvasculature, and neural coordination.

Description

The project aims to generate mechanistic insights into how beta cells influence surrounding tissues to coordinate activity across pancreas compartments in type 1 diabetes. It hypothesizes that insulin signaling affects exocrine tissue, microvasculature, and neural inputs, and that deterioration of beta cell control leads to pathological changes. The research involves manipulating insulin signaling in mouse models and studying human pancreas slices.

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