Glucagon receptor

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Glucagon Receptor[edit | edit source]

Illustration of glucagon binding to its receptor.

The glucagon receptor is a G protein-coupled receptor (GPCR) that binds the peptide hormone glucagon. It plays a crucial role in glucose metabolism by mediating the effects of glucagon, which is secreted by the alpha cells of the pancreas in response to low blood glucose levels.

Structure[edit | edit source]

The glucagon receptor is a member of the class B family of GPCRs. It is composed of seven transmembrane helices, an extracellular N-terminus, and an intracellular C-terminus. The receptor's structure allows it to interact with glucagon and initiate a signaling cascade inside the cell.

Function[edit | edit source]

Upon binding glucagon, the glucagon receptor activates adenylate cyclase through the Gs protein, leading to an increase in cyclic AMP (cAMP) levels. This rise in cAMP activates protein kinase A (PKA), which in turn phosphorylates various target proteins to regulate glycogenolysis, gluconeogenesis, and lipolysis. These processes increase blood glucose levels, providing energy to the body during fasting or between meals.

Signaling Pathway[edit | edit source]

The glucagon receptor signaling pathway involves several key steps:

1. Glucagon Binding: Glucagon binds to the extracellular domain of the receptor. 2. G Protein Activation: The receptor undergoes a conformational change, activating the associated Gs protein. 3. Adenylate Cyclase Activation: The Gs protein stimulates adenylate cyclase, increasing cAMP production. 4. PKA Activation: Elevated cAMP levels activate PKA. 5. Phosphorylation of Target Proteins: PKA phosphorylates enzymes involved in glucose production and release.

Clinical Significance[edit | edit source]

Dysfunction of the glucagon receptor can lead to metabolic disorders. Overactivity may contribute to hyperglycemia in type 2 diabetes mellitus, while underactivity can result in hypoglycemia. Understanding the receptor's role in glucose homeostasis is crucial for developing therapeutic strategies for these conditions.

Related Pages[edit | edit source]


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