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The kinase has been shown to stimulate Na<jats:sup>+<\/jats:sup>-coupled glucose transport in vitro and mediate the stimulation of electrogenic intestinal glucose transport by glucocorticoids in vivo. SGK1 expression is confined to glomerula and distal nephron in intact kidneys but may extend to the proximal tubule in diabetic nephropathy. To explore whether SGK1 modifies glucose transport in diabetic kidneys, Akita mice ( akita<jats:sup>+\/\u2212<\/jats:sup>), which develop spontaneous diabetes, have been crossbred with gene-targeted mice lacking SGK1 on one allele ( sgk1<jats:sup>+\/\u2212<\/jats:sup>) to eventually generate either akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>or akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>+\/+<\/jats:sup>mice. Both akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>and akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>+\/+<\/jats:sup>mice developed profound hyperglycemia (&gt;20 mM) within \u223c6 wk. Body weight and plasma glucose concentrations were not significantly different between these two genotypes. However, urinary excretion of glucose and urinary excretion of fluid, Na<jats:sup>+<\/jats:sup>, and K<jats:sup>+<\/jats:sup>, as well as plasma aldosterone concentrations, were significantly higher in akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>than in akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>+\/+<\/jats:sup>mice. Studies in isolated perfused proximal tubules revealed that the electrogenic glucose transport was significantly lower in akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>than in akita<jats:sup>+\/\u2212<\/jats:sup>\/ sgk1<jats:sup>+\/+<\/jats:sup>mice. 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