Abstract
The work reviewed above provides evidence that enhanced phospholipid turnover in islets may be a determinant of the secretory response to nutrient secretagogues and certain neurotransmitter and hormonal stimuli. The available data are compatible with the hypothesis that stimulated phospholipid turnover may be involved in the control of calcium mobilisation in islets, although additional possibilities clearly exist, such as the facilitation of membrane fusion during exocytosis and the liberation of arachidonic acid for subsequent metabolism via the cyclo-oxygenase and lipoxygenase pathways. Phospholipid and protein methylation may also be involved at some stage in stimulus-secretion coupling in pancreatic islets. Continued investigation of these topics is likely to contribute to a better understanding of the control of secretory activity in pancreatic islets, which in turn may throw light on pathophysiological aspects of islet function and perhaps suggest novel therapeutic approaches.
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