Patients with non-insulin-dependent diabetes mellitus have enlarged islets of Langerhans, an increased number of insulin-secreting beta cells, and a "horseshoe-shaped" relationship between plasma insulin and glucose levels. To some extent, beta-cell dysfunction in patients with type II diabetes is reversible with appropriate hypoglycemic therapy. Defects in the glucagon-secreting alpha cells in patients with non-insulin-dependent diabetes mellitus include basal hyperglucagonemia, an exaggerated glucagon response to aminogenic stimuli, and hyposuppressibility of glucagon by hyperglycemia. Although peripheral resistance to insulin may play a role in type II diabetes, defects in islet-cell function clearly play a significant role as well.
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