Insulin secretion from β-cells of pancreatic islets of Langerhans is primarily controlled by glucose or other nutrient secretagogues, and modified by a variety of hormones and neurotransmitters. The stimulation of insulin secretion by nutrient secretagogues requires the metabolism of the nutrient within the β-cell, the generation of ATP, which leads to the closure of ATP-sensitive K+ channels with the consequent depolarization of the cell, the opening of voltage-dependent Ca2+ channels and the influx of extracellular Ca2+ (reviewed by Ashcroft, 1988). Secretory responses to non-nutrient secretagogues are mediated by conventional cell-surface receptors linked to effector enzymes which regulate intracellular concentrations of cyclic AMP, diacylglycerol (DAG) and d-myo-inositol 1,4,5 trisphosphate (IP3) (reviewed by Prentki & Matschinsky, 1987). In addition to these second messengers, evidence is accumulating that another product of phospholipid hydrolysis, arachidonic acid (AA), may be involved in the regulation of insulin secretion (reviewed by Turk et al. 1987; Metz, 1988a).
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