Incretin
Overview[edit | edit source]
Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. They are released after eating and augment the secretion of insulin released from the pancreatic beta cells of the islets of Langerhans. The two main incretins in humans are glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), also known as glucose-dependent insulinotropic polypeptide.
Function[edit | edit source]
Incretins play a crucial role in the regulation of insulin secretion. They enhance the insulin response to oral glucose intake, a phenomenon known as the "incretin effect." This effect is responsible for the greater insulin response to oral glucose compared to intravenous glucose. Incretins also slow gastric emptying, inhibit glucagon release, and promote satiety, thereby contributing to the regulation of postprandial glucose levels.
Mechanism of Action[edit | edit source]
Incretins exert their effects by binding to specific receptors on the surface of pancreatic beta cells. GLP-1 binds to the GLP-1 receptor, while GIP binds to the GIP receptor. This binding activates intracellular signaling pathways that lead to increased insulin secretion. Additionally, GLP-1 has been shown to have protective effects on beta cells, promoting their survival and proliferation.
Degradation[edit | edit source]
Incretins are rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4). This enzyme cleaves the incretins, rendering them inactive. The short half-life of incretins in the bloodstream is due to this rapid degradation, which limits their physiological effects.
Clinical Significance[edit | edit source]
The incretin system is a target for the treatment of type 2 diabetes mellitus. DPP-4 inhibitors, also known as gliptins, are a class of oral hypoglycemics that prolong the action of incretins by inhibiting their degradation. This results in increased insulin secretion and decreased glucagon levels, leading to improved glycemic control.
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