期刊
DISEASE MODELS & MECHANISMS
卷 3, 期 9-10, 页码 567-580出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dmm.003210
关键词
-
资金
- NIH [R0161395, P50MH066172, Welch I-1382, R01CA118240, DK079862]
- JDRF [1-2008-16, 99-2007-472]
Diabetes is characterized by the loss, or gradual dysfunction, of insulin-producing pancreatic. beta-cell. Although. beta-cells can replicate in younger adults, the available diabetes therapies do not specifically target. beta-cell regeneration. Novel approaches are needed to discover new therapeutics and to understand the contributions of endocrine progenitors and. beta-cell regeneration during islet expansion. Here, we show that the regulators of G protein signaling Rgs16 and Rgs8 are expressed in pancreatic progenitor and endocrine cells during development, then extinguished in adults, but reactivated in models of both type 1 and type 2 diabetes. Exendin-4, a glucagon-like peptide 1 (Glp-1)/ incretin mimetic that stimulates. beta-cell expansion, insulin secretion and normalization of blood glucose levels in diabetics, also promoted re-expression of Rgs16::GFP within a few days in pancreatic ductalassociated cells and islet. beta-cells. These findings show that Rgs16::GFP and Rgs8::GFP are novel and early reporters of G protein-coupled receptor (GPCR)-stimulated. beta-cell expansion after therapeutic treatment and in diabetes models. Rgs16 and Rgs8 are likely to control aspects of islet progenitor cell activation, differentiation and. beta-cell expansion in embryos and metabolically stressed adults.
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