Low Glucose Enhances Na + /Glucose Transport in Bovine Brain Artery Endothelial Cells

• DOI: 10.1161/01.str.29.4.844
• Publication Date: 2011-06-17T20:10:52Z
• Authors: Tomoyuki Nishizaki; Toshiyuki Matsuoka
• Keywords: Phlorizin; GLUT3; Carbohydrate Metabolism

Brain arteries are structurally characterized by the tight junctions of endothelium and no vasa vasorum that feed themselves. This raises question how brain provided with glucose. A possible explanation is glucose uptake into may be mediated both GLUT1, a facilitative transporter, Na+/glucose cotransporter (SGLT)-like transporter. The functional role for SGLT-like however, unknown. In present study we investigated transporter-operated arterial endothelial cells recording glucose-evoked Na+ currents monitoring [3H]-2-deoxy-D-glucose ([3H]-2-DOG).Endothelial were cultured from bovine cerebral cortical arteries. Whole-cell patches made to cells, recorded. Cells incubated [3H]-2-DOG, was determined liquid scintillation counter.Glucose alpha-methyl-D-glucoside (alphaMeDG), specific compound SGLTs, evoked in whole-cell voltage-clamp configuration, enhanced over 30 minutes' preincubation glucose-free media. Glucose-induced inhibited alphaMeDG, selective SGLT inhibitor phlorizin, dinitrophenol (DNP), an energy metabolism, or deletion extracellular solution, which indicates Na+- energy-dependent Notably, desensitized, reduced concentration-dependent manner, markedly either second application addition patch electrode filling solution; they potentiated, treatment cytochalasin B, GLUT1 GLUT5 inhibitor. Consistent results patch-clamp recordings, [3H]-2-DOG insult, enhancement transporter.The presented demonstrate transporter takes part artery regulated intracellular concentrations; insult ensuing low cytosolic enhance activity thus important maintenance adequate concentration wall under conditions stress, such as hypoglycemia.