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however, metabolically stressed Glp1r cell/ :Gcgr cell/ mice exhibit impaired oral and IP glucose intolerance as compared to HFD-fed controls ( + alpha-cells, and a greater dependency on GLP-1R signaling for insulin secretion, as compared to islets from healthy donors ( + :glucagon + alpha-cells with the onset of diabetes in db/db mice as compared to normal mice ( Psammomys obesus , a rodent model of nutritionally induced diabetes, document an increase in islet GLP-1 production in response to the development of symptoms of T2DM ( Figure 4 Considering that chronic beta-cell GLP-1R signaling activates cAMP-responsive element binding (CREB) and epidermal growth factor receptor (EGFR) pathways that induce pro-survival and anti-apoptotic responses ( Figure 4 )
10.1161/CIRCRESAHA.119.316337 Circ Res
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Annu Rev Physiol (2023) 85:26991
30 MulcahyH.MazenodL
