Abstract

The presence of oscillations in peripheral insulin concentrations has sparked a number of studies evaluating the impact of the insulin release pattern on the action of insulin on target organs. These have convincingly shown that equal amounts of insulin presented to target organs have improved action when delivered in a pulsatile manner. In addition, impaired (not absent) pulsatility of insulin secretion has been demonstrated in Type II (non-insulin-dependent) diabetes mellitus, suggesting a possible mechanism to explain impaired insulin action in Type II diabetes. Whereas the regulation of overall insulin secretion has been described in detail, the mechanisms by which this regulation affects the pulsatile insulin secretory pattern, and the relative and absolute contribution of changes in the characteristics of pulsatile insulin release have not been reviewed previously. This review will focus on the importance of the secretory bursts to overall insulin release, and on how insulin secretion is adjusted by changes in these secretory bursts. Detection and quantification of secretory bursts depend on methods, and the methodology involved in studies dealing with pulsatile insulin secretion is described. Finally, data suggest that impaired pulsatile insulin secretion is an early marker for beta-cell dysfunction in Type II diabetes, and the role of early detection of impaired pulsatility to predict diabetes or to examine mechanisms to cause beta-cell dysfunction is mentioned.