What effect does gastric inhibitory peptide have on insulin and glucagon?

Gastric inhibitory peptide (GIP), also known as glucose-dependent insulinotropic polypeptide, plays a significant role in glucose metabolism and appetite regulation. Following the ingestion of food, particularly when carbohydrates are consumed, GIP is secreted by K cells in the duodenum and jejunum.

GIP primarily stimulates the release of insulin from the pancreas in response to elevated blood glucose levels, facilitating the uptake of glucose by cells. However, it is essential to note that GIP also has an inhibitory effect on glucagon secretion. Glucagon, produced by alpha cells in the pancreas, is responsible for increasing blood glucose levels by promoting gluconeogenesis and glycogenolysis in the liver. When blood glucose levels rise after a meal, the secretion of glucagon needs to be inhibited to prevent the liver from releasing more glucose into the bloodstream and to maintain glucose homeostasis.

Thus, GIP acts to inhibit the secretion of both insulin in certain contexts (when insulin levels are sufficiently high) and glucagon, creating an effective system that helps regulate glucose levels after meals. This dual action is vital for ensuring that insulin and glucagon levels are balanced, promoting optimal metabolic responses after nutrient intake. Therefore, the correct understanding is that gastric inhibitory peptide