Roles of glucose-dependent insulinotropic polypeptide in diet-induced obesity

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretins that play an important role in glucose metabolism, by increasing glucose-induced insulin secretion from pancreatic beta-cells and help regulate bodyweight. Although they show a similar action on glucose-induced insulin secretion, two incretins are distinct in various aspects. GIP is secreted from enteroendocrine K cell mainly expressed in the upper small intestine, and GLP-1 is secreted from enteroendocrine L cells mainly expressed in the lower small intestine and colon by the stimulation of various nutrients. The mechanism of GIP secretion induced by nutrients, especially carbohydrates, is different from that of GLP-1 secretion. GIP promotes fat deposition in adipose tissue, and contributes to fat-induced obesity. In contrast, GLP-1 participates in reducing bodyweight by suppressing food consumption and/or slowing gastric emptying. There is substantial evidence that GIP and GLP-1 might differently contribute to bodyweight control. Although meal contents influence both glycemic and weight control, we do not fully understand whether incretin actions differ depending on the contents of the meal and what kind of signaling is involved in its context. We focus on the molecular mechanism of GIP secretion induced by nutrients, as well as the roles of GIP in weight changes caused by various diets.

Automated summary

This article introduces the different roles of GIP and GLP-1 in glucose metabolism and weight regulation. GIP is mainly secreted in the upper small intestine, while GLP-1 is mainly secreted in the lower small intestine and colon. GIP promotes fat deposition while GLP-1 suppresses food consumption and gastric emptying.