Clinical implications of amylin and amylin deficiency

This paper presents an overview of the physiology of glycemic control and the mechanisms of amylin deficiency in people with diabetes. Benefits of replacement therapy with both pramlintide and insulin are discussed.

The discovery of the pancreatic beta-cell hormone amylin, which is cosecreted with insulin in response to hyperglycemia, has prompted a reanalysis of the mechanisms underlying the control of glucose homeostasis. A review of the current literature on amylin and amylin deficiency provides the basis of this reanalysis, with a discussion of the clinical implications for people with diabetes.

Amylin appears to work with insulin to regulate plasma glucose concentrations in the bloodstream, suppressing the postprandial secretion of glucagon and restraining the rate of gastric emptying. People with diabetes have a deficiency in the secretion of amylin that parallels the deficiency in insulin secretion, resulting in an excessive inflow of glucose into the bloodstream during the postprandial period.

While insulin replacement therapy is a cornerstone of diabetes treatment, replacement of the function of both amylin and insulin may allow a more complete restoration of the normal physiology of glucose control.