This review presents recent concepts of how ??-agonists affect glucose homeostasis by modulating insulin secretion, liver metabolism, and uptake of glucose into muscle, with attention to the influence of hypoglycemia on ??-agonist sensitivity and the effects of ??3-adrenergic receptor (??3AR) polymorphisms on adipocyte metabolism. Specific ??2-agonist effects on the pancreatic ?? cell result in increased insulin secretion, yet other mechanisms, such as increased glucagon secretion and hepatic effects, cause an overall increase in serum glucose and an apparent decrease in insulin sensitivity. Human studies confirm the presence of ??2ARs on pancreatic ?? cells. Intensive treatment of diabetes mellitus with insulin, especially in type 1 diabetes, has led to increased incidence of hypoglycemia. Repeated episodes of hypoglycemia lead to unawareness of neuroglycopenia, a major limitation to intensive treatment. Hypoglycemic unawareness is associated with reduced ??-agonist sensitivity. Scrupulous avoidance of hypoglycemia over many weeks to months can restore ??-agonist sensitivity and improve detection of hypoglycemia. ??-agonists have also been employed to prevent hypoglycemia. ??-agonists can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. While ??1ARs and ??2ARs mediate many of these actions, it is likely that ??3ARs in the adipocyte membrane also play an important role. Specific ??3AR subtypes have been associated with obesity and the metabolic syndrome.
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