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The endocrine part of the pancreas plays a central role in blood-glucose regulation. It is well established that an elevation of glucose concentration reduces secretion of the hyperglycaemia-associated hormone glucagon from pancreatic alpha 2 cells. The mechanisms involved, however, remain unknown. Electrophysiological studies have demonstrated that alpha 2(More)
Microfluorimetric and patch-clamp techniques have been combined to determine the relationship between changes in mitochondrial metabolism, the activity of KATP channels and changes in intracellular free calcium concentration ([Ca2+]i) in isolated pancreatic beta-cells in response to glucose, ketoisocaproic acid (KIC) and the electron donor couple(More)
Membrane potential and membrane currents were recorded from single mouse pancreatic beta-cells using the perforated patch whole-cell recording technique at 30 degrees C. Single beta-cells maintained in primary tissue culture exhibited glucose-dependent electrical activity similar to that reported for freshly isolated intact islets. The resting input(More)
1. The whole-cell and outside-out patch configurations of the patch-clamp technique were used to investigate the effects of extracellular tetraethylammonium ions (TEA+) and quinine on both Ca2(+)-activated and ATP-regulated K+ channels in mouse pancreatic beta-cells. 2. The Ca2(+)-activated K+ channel has a single-channel K+ permeability of 4.7 x 10(-13)(More)
A cDNA clone encoding an inwardly-rectifying potassium channel subunit (Kir6.2) was isolated from an insulinoma cDNA library. The mRNA is strongly expressed in brain, skeletal muscle, cardiac muscle and in insulinoma cells, weakly expressed in lung and kidney and not detectable in spleen, liver or testis. Heterologous expression of Kir6.2 in HEK293 cells(More)
1. The whole-cell and outside-out patch configurations of the patch-clamp technique were used to study the mechanisms of block produced by external tetraethylammonium ions (TEA+) and quinine on delayed rectifying K+ channels in mouse pancreatic beta-cells. 2. In whole-cell recordings, TEA+ blocks the delayed outward current (which reflects the activity of(More)
1. To investigate the mechanisms regulating the reuptake of secretory granule membranes following regulated exocytosis, we have monitored changes in cell capacitance in single pancreatic beta-cells. 2. Membrane retrieval (endocytosis) occurred both in a continuous manner and in abrupt steps, corresponding to the simultaneous retrieval of 50-100 granules.(More)
Glucose stimulates insulin secretion from the pancreatic beta-cell by increasing the cytosolic calcium concentration. It is believed that this increment results mainly from Ca2+ influx through dihydropyridine-sensitive calcium channels because insulin secretion is abolished by dihydropyridine antagonists and is potentiated by dihydropyridine agonists.(More)
1. We have investigated the mechanism by which L-arginine stimulates membrane depolarization, an increase of intracellular calcium ([Ca2+]i) and insulin secretion in pancreatic beta-cells. 2. L-Arginine failed to affect beta-cell metabolism, as monitored by NAD(P)H autofluorescence. 3. L-Arginine produced a dose-dependent increase in [Ca2+]i, which was(More)
The contribution of Ca2(+)-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic beta-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2(+)-dependent component could be identified by its rapid inactivation and(More)