Insulin and Amylin: Restoring Balance in Glycemic Control

Wednesday, August 10, 2005

Corporate-sponsored Symposium

Supported by an educational grant from Amylin Pharmaceuticals, Inc.

Faculty
Catherine Martin, MS, APRN, BC-ADM, CDE
Steven V Edelman, MD
Susan K Owen, RN, MSN, CDE
Laura Want, RN MS, CDE, BC-ADM

Reported by Joelle Escoffery, PhD

For many years, glucose homeostasis was thought to be a function of the hormones insulin and glucagon. However, late in the last century, the second β-cell hormone amylin was discovered. Amylin, along with glucagon-like peptide-1 and cholecystokinin, is responsible for the regulation of meal-derived glucose, whereas insulin and glucagon play an important role in endogenous glucose production. Amylin is absent in people with type 1 diabetes and deficient in people with insulin-requiring type 2 diabetes. When used in conjunction with insulin, amylin has been shown to improve postprandial glucose control, decrease postprandial glucagon secretion, regulate gastric emptying, and promote satiety.

Clinical research with pramlintide, a synthetic amylin analog, has demonstrated a number of beneficial therapeutic effects. When pramlintide was used in conjunction with insulin therapy in people with type 1 diabetes and insulin-requiring type 2 diabetes, improvements in postprandial glucose control and weight loss were observed. In early research, pramlintide was associated with an increased incidence of hypoglycemia. However, this finding seems to be largely attributable to the fact that insulin dose was not titrated in the initial studies. Current recommendations suggest a 50% reduction in mealtime insulin when initiating pramlintide therapy. Other important clinical considerations with pramlintide use include appropriate patient selection and dose titration to decrease the incidence of nausea.