Glucose-induced increase in cytoplasmic pH in pancreatic beta-cells is mediated by Na+/H+ exchange, an effect not dependent on protein kinase C.

Journal article

Glucose-induced changes in cytoplasmic pH (pHi) were investigated using pancreatic beta-cells isolated from obese hyperglycemic mice. Glucose, at concentrations above 3-5 mM, depolarized the beta-cell and increased pHi, cytoplasmic free Ca2+ ([Ca2+]i), and insulin release. This increase in pHi was dependent on the presence of extracellular Na+ and was inhibited by 5-(N-ethyl-N-isopropyl) amiloride, a blocker of Na+/H+ exchange. Stimulation of protein kinase C with phorbol ester also induced a...

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Authors: Juntti-Berggren, L; Arkhammar, P; Nilsson, T; Rorsman, P; Berggren, P

• Publication status: Published
• Journal: Journal of biological chemistry
• Volume: 266
• Issue: 35
• Pages: 23537-23541
• Publication date: 1991-12-01
• EISSN: 1083-351X
• ISSN: 0021-9258
• Language: English
• Keywords: Insulin; Cells, Cultured; Tetradecanoylphorbol Acetate; Potassium; Ammonium Chloride; Mice; Membrane Potentials; Mice, Obese; Carrier Proteins; Kinetics; Amiloride; Tolbutamide; Calcium; Animals; Sodium; Glucose; Hydrogen-Ion Concentration; Protein Kinase C; Islets of Langerhans; Sodium-Hydrogen Antiporter