Abstract
Hyperinsulinemia is a well-recognized if incompletely understood concomitant of obesity. Diminished sensitivity to the effects of insulin on glucose uptake and metabolism in skeletal muscle, commonly referred to as "insulin resistance," is known to contribute to the hyperinsulinemia of obesity by evoking an increase in pancreatic insulin secretion in order to maintain euglycemia. Decreased hepatic extraction of insulin in obese persons appears to be involved as well, as a consequence of increased levels of free fatty acids in the portal blood.1 A primary increase in insulin secretion mediated by the pancreatic nerves, and a secondary increase in response to excessive . . .