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Anion fluxes, volume regulation and electrical activity in the mammalian pancreatic beta‐cell

The secretion of insulin from the pancreatic f-cell can be influenced, as with numerous endocrine cell types, by hormones, neurotransmitters and drugs which bind to cell surface receptors and generate an intracellular signal (e.g. cyclic AMP, inositol 1,4,5-trisphosphate). However, the ,-cell has in addition the uncommon, possibly unique, ability to increase its hormone output in response to a rise in the ambient concentration of nutrients, notably glucose. Insulin release in response to virtually any type of stimulus is intimately associated with altered electrical activity. For example, a rise in glucose concentration within the approximate range 5-20 mM results in a progressive increase in the intensity of electrical, and hence secretory, activity. This, and virtually all other effects of glucose on the fl-cell, require metabolism of the sugar and the generation of some intracellular metabolic signal(s), the precise identity of which is unknown. The nature and regulation of/-cell electrical activity is a complex subject which has been extensively reviewed (for example, see Ashcroft & Rorsman, 1989; Cook, Satin & Hopkins, 1991). The majority of studies of f-cell electrophysiology have employed mouse islets or f-cells, and it is becoming apparent that profound species differences exist. In mouse fl-cells exposed to intermediate glucose concentrations, a rhythmic 'bursting' pattern is seen, consisting of a depolarization of the membrane potential, leading to bursts of Ca2+-dependent action potentials followed by a repolarization leading to a silent phase. As the glucose concentration progressively rises, the duration of the bursts