Insulin resistance and compensatory hyperinsulinemia are commonly present in obesity. The biochemical mechanisms responsible for the maintenance of basal hypersecretion of insulin are reviewed in this article. Under basal, fasting and fed conditions the hyperinsulinemia of obesity largely depends on increased insulin secretion, without any alteration of the temporal secretion. This suggests that the functioning beta cell mass is enhanced, but normal regulatory mechanisms are maintained. A number of alterations in beta-cell function are present in conditions of impaired glucose tolerance which precede the onset of overt diabetes.