Journal
DIABETES OBESITY & METABOLISM
Volume 11, Issue -, Pages 180-188Publisher
WILEY
DOI: 10.1111/j.1463-1326.2009.01108.x
Keywords
cAMP; Epac2; cAMP-GEFII; incretin; insulin; Rap1
Categories
Funding
- Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology
Ask authors/readers for more resources
Insulin secretion is regulated by a series of complex events generated by various intracellular signals including Ca2+, ATP, cAMP and phospholipid-derived signals. Glucose-stimulated insulin secretion is the principal mode of insulin secretion, and the mechanism potentiating the secretion is critical for physiological responses. Among the various intracellular signals involved, cAMP is particularly important for amplifying insulin secretion. Recently, glucagon-like peptide-1 (GLP-1) analogues and dipeptidyl peptidase-IV (DPP-IV) inhibitors have been developed as new antidiabetic drugs. These drugs all act through cAMP signalling in pancreatic beta-cells. Until recently, cAMP was generally thought to potentiate insulin secretion through protein kinase A (PKA) phosphorylation of proteins associated with the secretory process. However, it is now known that in addition to PKA, cAMP has other targets such as Epac (also referred to as cAMP-GEF). The variety of the effects mediated by cAMP signalling may be linked to cAMP compartmentation in the pancreatic beta-cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available