ABSTRACT
The 3',5'-cyclic adenosine monophosphate (cAMP) is a classic second messenger that is intimately involved in the regulation of food intake and body weight at the hypothalamus as well as insulin secretion from the pancreatic β-cells. The transgenic Rat Insulin Promoter-phosphodiesterases 3B (RIP-PDE3B) mouse model has been useful in shedding new light on the physiological significance of regulation of cAMP by PDE3B in pancreatic β-cells, particularly with respect to its roles in glucose-and Glucagon-like peptide-1-stimulated insulin secretion. The evidence summarized so far strongly suggests that regulation of cAMP level at the hypothalamus is critical to the control of energy homeostasis. The genetic studies from the RIP-PDE3B mouse model also suggest that cAMP is important in preventing or delaying the development of fatty diet–induced insulin resistance. The evidence gathered so far suggests that the phosphoinositide-3-kinase-PDE3B-cAMP pathway is a critical signaling mechanism in the broad scheme of food-intake control.
