Both GLP1 and GIP promote insulin biosynthesis, insulin secretion, and islet β cell survival. GLP1 exerts additional actions important for regulation of glucose homeostasis, including inhibition of glucagon secretion and gastric emptying, and induction of satiety. GIP, but not GLP1, directly engages receptors on adipocytes coupled to energy storage. In contrast, CCK and gastrin do not seem to acutely regulate levels of plasma glucose but might be important for stimulating the formation of new β cells by stimulating islet neogenesis.