Glucose promotes turnover of Na+ in pancreatic beta-cells.
Ouabain-induced changes of the free cytoplasmic Na+ concentration ([Na+]i) were monitored in aggregates of cells prepared from beta-cell-rich pancreatic mouse islets and the results were compared with the total islet content of sodium. The steady-state [Na+]i was lower in 20 mM glucose (11 mM) than in 3 mM glucose (14 mM). In the presence of 3 mM glucose the addition of 1 mM ouabain resulted in a rise in [Na+]i with an initial rate of 1.5 mM/min. However, the increase of total sodium corresponded to 2.8 mM/min, suggesting that rapid binding and/or sequestration of Na+ are prominent features for pancreatic beta-cells. Elevation of the glucose concentration to 20 mM increased the rate of ouabain-dependent rise of [Na+]i. The effect of glucose was mimicked by 1 mM tolbutamide or 100 microM carbachol and was counteracted by 100 nM of the alpha 2-adrenergic agonist clonidine. Glucose also accelerated the lowering of [Na+]i after withdrawal of ouabain. In promoting not only the entry but also the extrusion of Na+, glucose actually enhances the turnover of the ion in pancreatic beta-cells.
Saha
S
S
Department of Medical Cell Biology, Uppsala University, Sweden.
Grapengiesser
E
E
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000378:metabolism*; D051379:Mice; D012964:Sodium / Q000378:metabolism*
D012964:Sodium; D005947:Glucose