title: Roles of amylin in diabetes and in regulation of nutrient load.
abstract: In summary, amylin, via its hormonal actions, may be relevant to the treatment of both forms of diabetes, and, paradoxically, via its amyloidogenic properties, may also be relevant to the pathogenesis of NIDDM. Amylin potently inhibits postprandial glucagon secretion. The absence of this action could contribute to the hyperglucagonemia and subsequently, excessive endogenous glucose production, fasting hyperglycemia, and propensity to ketosis seen in insulinopenic diabetes. Restoration of normal glucagon secretion by amylin replacement therapy could therefore be therapeutically important in treatment of insulin-dependent diabetes mellitus. Amylin potently inhibits gastric emptying. This action is consistent with a physiologic role of amylin to regulate carbohydrate absorption. Of peptides known to be secreted in response to ingested carbohydrate, only amylin and glucagon-like peptide-1 are reported to inhibit gastric emptying at near-physiologic concentrations, and could therefore participate in nutrient-mediated feedback control of carbohydrate release from the stomach. Amylin reduces food intake in rodents. This action, which synergizes with a similar action of CCK, could reflect a role as short-term peripheral satiety agent. Amylin alone or in combination with CCK may be useful in moderating caloric intake in obesity and other metabolic disorders. Although insulin has been extensively studied as a therapy and as a controller of nutrient storage and metabolism, the role of its beta-cell partner, amylin, has been largely unrecognized. In contrast to the nutrient disposal and storage role of insulin, amylin appears to more generally address the opposite side of the energy balance equation, the assimilation of nutrient.
authors.forename: A
authors.initials: A
authors.lastname: Young
authors.forename: M
authors.initials: M
authors.lastname: Denaro
mesh_terms: D000682:Amyloid / Q000502:physiology*; D000818:Animals; D003920:Diabetes Mellitus / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D004435:Eating / Q000502:physiology; D005746:Gastric Emptying / Q000502:physiology; D005934:Glucagon / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D058228:Islet Amyloid Polypeptide; D007515:Islets of Langerhans / Q000503:physiopathology; D009747:Nutritional Physiological Phenomena / Q000502:physiology*
chemical_list: D000682:Amyloid; D007328:Insulin; D058228:Islet Amyloid Polypeptide; D005934:Glucagon