Optimizing diabetes treatment using an amylin analogue.
Diabetes treatment has traditionally focused on correcting insulin deficiency using exogenous insulin and oral agents to enhance insulin secretion or insulin sensitivity in peripheral tissues. The more recent view of diabetes as a disease that affects multiple hormones, including insulin, has led to the development of therapies more broadly aimed at restoring glucose homeostasis by correcting abnormalities in other glucoregulatory hormones, including amylin. Patients with diabetes are deficient in both insulin and amylin, which contributes to postprandial hyperglycemia. Amylin, a neuroendocrine hormone secreted in response to nutrient intake, suppresses postprandial glucagon secretion, regulates gastric emptying, and regulates appetite. Pramlintide, a synthetic analog of the beta cell hormone amylin, regulates the rate of appearance of glucose in the bloodstream after meals through several mechanisms of action: slowing gastric emptying, preventing inappropriate postprandial secretion of glucagon, and increasing satiety. Long-term studies have demonstrated that pramlintide improves postprandial glucose fluctuations and glycosylated hemoglobin levels while reducing the amount of insulin needed and body weight. This combination of benefits associated with pramlintide makes it an attractive treatment option for patients with either type 1 or type 2 diabetes.
Edelman
Steven V
SV
University of California San Diego, Veterans Affairs Medical Center, 3350 La Jolla Village Drive (111G), San Diego, CA 92161, USA.
D000682:Amyloid / Q000009:adverse effects / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D003920:Diabetes Mellitus / Q000188:drug therapy*; D007004:Hypoglycemic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D058228:Islet Amyloid Polypeptide; D012449:Safety
D000682:Amyloid; D007004:Hypoglycemic Agents; D058228:Islet Amyloid Polypeptide; D002097:C-Reactive Protein; C105254:pramlintide