Abstract

Rashidul Haque* and Sultana Rajia

ABSTRACT

In normal physiological condition, the pancreatic beta cells continuously monitor the blood sugar level and other fuel levels and, in response, secrete insulin to maintain normal fuel homeostasis. During the postpartum period, high plasma glucose level quickly stimulate beta cells to secrete insulin in order to decrease hepatic glucose output and promote glucose uptake in other tissues, particularly muscle and adipose tissue. The mitochondria of the pancreatic beta cells play a major role in this process. In addition to producing energy in the form of ATP to support insulin secretion, they also synthesize metabolites (anapleros) that can act as factors that couple glucose sensing to insulin granule exocytosis. ATP itself, and possibly modulated by these coupling factors, closes ATP-sensitive potassium channels, causing membrane depolarization that increases intracellular calcium to cause insulin secretion. In this review, we have discussed many of the biochemical pathways and the role of ATP-sensitive potassium channels in the regulation of glucose-stimulated insulin secretion (GSIS), which has attracted many scientists in the recent times to work in diabetic research.