RESUMO
Normally, the release of glucagon is halted at the beginning of a meal by a direct mechanism: insulin secretion from the beta cells within the pancreas inhibits the release of glucagon from the beta cells. An "indirect" mechanism--amylin (a neuroendocrine hormone also secreted from the beta cells)--suppresses the release of glucagon through the central nervous system. In type 2 diabetes, the first phase insulin release is absent, and as amylin is released in direct proportion to insulin, both mechanisms to suppress glucagon are absent. The result is that glucagon secretion and, ultimately, the stimulation of hepatic glucose release continue, resulting in extreme postprandial hyperglycemia. It has been shown that amylin supplementation with injections of the human amylin analogue pramlintide, in patients with insulin-requiring type 2 diabetes, helps limit postprandial hyperglycemia. Amylin supplementation not only suppresses glucagon secretion but also slows the absorption of glucose in the intestines and limits nutrient intake by providing a feeling of satiety, resulting in a moderate reduction in body weight for many patients. Recently approved by the FDA, pramlintide is now available for clinical use. However, it is important that pramlintide be prescribed only for selected patients and that these patients are thoroughly educated in the use of this agent, especially during initiation of treatment. Patients suited to pramlintide use are those who have not achieved adequate glycemic control despite optimal insulin use, are under the care of a professional health care provider skilled in the use of insulin and a diabetes educator, and are well-disciplined in diabetes self-management.
