Building Competency in Diabetes Education THE ESSENTIALS

3-8 | CHAPTER 3

(10). These peptide hormones, are produced at low basal levels in a fasting state (10). The incretin effect was first described as a greater insulin response when glucose was administered orally as compared to intravenously, suggesting that these gut hormones have important effects in augmenting glucose-dependent insulin release (8). GIP and GLP-1 (8,10) • Stimulates beta cell proliferation. • Suppresses glucagon secretion, decreasing hepatic glucose output and postprandial glucose levels. • Reduces food intake. • Regulates gastric emptying, thus limiting postprandial glucose rise. • Dipeptidyl peptidase-4 (DPP-4) rapidly inactivates endogenous GLP-1 (11). Amyloid polypeptide or Amylin (5,8) • Amylin, like insulin, is located within the beta cell and is co-secreted with insulin. • Complements the action of insulin and regulates the rate of gastric emptying to manage the rate of glucose appearance. • Influences the central nervous system to suppress postprandial glucagon and subsequent hepatic glucose production. • Is almost absent in type 1 diabetes (like insulin) and is reduced in type 2 diabetes. • Its physiological role is unclear at present. Glucagon, the liver and the counterregulatory response Glucose is the optimal fuel for muscle and adipose tissue, but these tissues may also use fatty acids and other substrates for energy (5). The brain, however, must have an ongoing supply of glucose, so the body has several defence mechanisms, known as the counterregulatory system, to help it cope with starvation and prevent hypoglycemia (12). The counterregulatory system consists of glucagon, catecholamines, growth hormone and glucocorticoids (12).