Glucagon-like peptide-1 receptor

Glucagon-like peptide-1 receptor (GLP-1R) is a G protein-coupled receptor that binds glucagon-like peptide-1 (GLP-1), a hormone involved in the regulation of blood glucose levels. The receptor is expressed in various tissues, including the pancreas, brain, and heart, and plays a crucial role in glucose homeostasis and cardiovascular function.

Structure

The GLP-1R is a member of the class B1 family of G protein-coupled receptors. It is a transmembrane protein composed of seven alpha-helical segments connected by three extracellular and three intracellular loops. The N-terminal domain of the receptor is responsible for ligand binding, while the C-terminal domain is involved in receptor activation and signal transduction.

Function

Upon binding of GLP-1, the GLP-1R activates the adenylate cyclase enzyme, leading to an increase in the intracellular concentration of cyclic AMP (cAMP). This, in turn, activates protein kinase A (PKA) and exchange protein directly activated by cAMP (EPAC), which mediate the downstream effects of GLP-1R activation.

In the pancreas, GLP-1R activation stimulates insulin secretion from beta cells in a glucose-dependent manner. In the brain, it promotes satiety and reduces food intake. In the heart, it improves cardiac function and protects against ischemic injury.

Clinical significance

GLP-1R is a target for the treatment of type 2 diabetes. GLP-1R agonists, such as exenatide and liraglutide, are used to increase insulin secretion, suppress glucagon release, and reduce appetite. These drugs have been shown to improve glycemic control and promote weight loss in patients with type 2 diabetes.

In addition, research is ongoing to explore the potential benefits of GLP-1R activation in the treatment of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and cardiovascular diseases.

See also

• Glucagon-like peptide-1
• G protein-coupled receptor
• Type 2 diabetes

This GPCR-related article is a stub. You can help WikiMD by expanding it.