Modulation of dihydropyridine-sensitive Ca2+ channels by glucose metabolism in mouse pancreatic beta-cells.

Journal article

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. Glucose may influence Ca2+ influx through these channels in two ways: either by regulating the beta-cell membrane potential or by biochemical modulation of the channel itself. The former mechanism is well established. Glucose metabolism, by closing ATP-sensitive K+ channels, depolarizes the beta-cell membrane and initiates Ca2+-dependent electrical activity, with higher glucose concentrations further increasing Ca2+ influx by raising the frequency of action potentials. We show here that glucose metabolism also increases calcium influx directly, by modulating the activity of dihydropyridine-sensitive Ca2+ channels.

Authors: Smith, P; Rorsman, P; Ashcroft, F

• Publication status: Published
• Journal: Nature
• Volume: 342
• Issue: 6249
• Pages: 550-553
• Publication date: 1989-11-01
• DOI: 10.1038/342550a0
• EISSN: 1476-4687
• ISSN: 0028-0836
• Language: English
• Keywords: Electric Conductivity; Animals; Islets of Langerhans; Glucose; Dihydropyridines; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; Calcium Channels; Membrane Potentials; Calcium; Mice