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Regulation of renal tubular glucose reabsorption by Akt2/PKB[beta]

Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBb influences the Na...-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis o...

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Published in:American journal of physiology. Renal physiology 2010-05, Vol.298 (5), p.F1113
Main Authors: Kempe, Daniela S, Siraskar, Gulab, Fröhlich, Henning, Umbach, Anja T, St¨ubs, Michael, Weiss, Florian, Ackermann, Teresa F, Völkl, Harald, Birnbaum, Morris J, Pearce, David, Föller, Michael, Lang, Florian
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Language:English
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Summary:Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBb influences the Na...-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2/PKBb (akt2...) and in their wild-type littermates (akt2...). Plasma glucose concentration was significantly higher in akt2... mice than in akt2... mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2... mice. Urinary glucose excretion was significantly higher in akt2... mice compared with akt2... mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2... mice than in those from akt2... mice. In conclusion, Akt2/PKBb plays a role in the regulation of renal glucose transport. (ProQuest: ... denotes formulae/symbols omitted.)
ISSN:1931-857X
1522-1466