Islet amyloid polypeptide

Also known as: Amylin, Diabetes-associated peptide, Insulinoma amyloid peptide, IAPP, P10997

**Mechanism of Action** Islet amyloid polypeptide (IAPP, amylin) is a 37-amino-acid peptide hormone co-secreted with insulin from pancreatic β-cells. It acts centrally via the area postrema and nucleus tractus solitarii to suppress glucagon secretion, slow gastric emptying, and promote satiety, thereby contributing to postprandial glucose regulation. IAPP also modulates peripheral insulin sensitivity and energy expenditure through interactions with calcitonin receptor-like receptors (CT-RAMP1/3). In pathological states, IAPP misfolds into toxic oligomers and amyloid fibrils, inducing β-cell apoptosis and contributing to islet dysfunction in type 2 diabetes. **Key Research Findings** Experimental studies demonstrate that IAPP aggregation is linked to β-cell loss and insulin resistance. Transgenic rodent models overexpressing human IAPP develop hyperglycemia and islet amyloid deposits, recapitulating features of type 2 diabetes. Conversely, IAPP receptor agonists (e.g., pramlintide) improve glycemic control by delaying gastric emptying and reducing postprandial glucagon. Research also implicates IAPP in energy homeostasis via hypothalamic signaling, with potential roles in obesity and metabolic syndrome. Current investigations focus on inhibitors of IAPP aggregation (e.g., small molecules, peptides) to preserve β-cell mass. **Clinical Relevance** Synthetic IAPP analogs (e.g., pramlintide) are FDA-approved as adjunctive therapy for type 1 and type 2 diabetes to improve postprandial glucose control. However, native IAPP’s amyloidogenic properties limit its therapeutic use. Experimental strategies targeting IAPP aggregation or receptor modulation are under preclinical evaluation for diabetes and obesity. No approved therapies directly address IAPP-mediated β-cell toxicity. For research purposes only — not medical advice.

Key data

Mechanism of action

Amylin/IAPP is a glucoregulatory peptide hormone that plays an important role in the regulation of energy homeostasis (PubMed:2690069). Selectively inhibits insulin-stimulated glucose utilization and glycogen deposition in muscle, while not affecting adipocyte glucose metabolism. IAPP function is mediated by the CALCR-RAMPs (AMYRs) receptor complexes (By similarity). Amylin can also bind CALCR receptor in the absence of RAMPs, although it is more selective for AMYRs (By similarity)

Research & studies

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