The therapeutic landscape of type 2 diabetes and obesity has evolved from single-hormone incretin modulation towards multireceptor metabolic engineering. Amylin is cosecreted with insulin from pancreatic β cells in response to food intake and acts on amylin receptors distributed across the brain, pancreas, adipose tissue, and gastrointestinal tract to regulate appetite, delay gastric emptying, and decrease glucagon secretion, providing multisite integrative control of energy balance.1,2 Notably, amylin receptors are heterodimeric complexes composed of a calcitonin receptor core and receptor activity-modifying proteins (RAMP1, RAMP2, or RAMP3).
Kaynak: The Lancet
