{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,12]],"date-time":"2023-10-12T18:48:25Z","timestamp":1697136505871},"reference-count":46,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:p>The phosphoinositide-dependent kinase-1 (PDK-1) activates the serum- and glucocorticoid-inducible kinase and protein kinase B isoforms, which, in turn, are known to stimulate the renal and intestinal Na<jats:sup>+<\/jats:sup>-dependent glucose transporter 1. The present study has been performed to explore the role of PDK-1 in electrogenic glucose transport in small intestine and proximal renal tubules. To this end, mice expressing \u223c20% of PDK-1 ( pdk1<jats:sup>hm<\/jats:sup>) were compared with their wild-type littermates ( pdk1<jats:sup>wt<\/jats:sup>). According to Ussing chamber experiments, electrogenic glucose transport was significantly smaller in the jejunum of pdk1<jats:sup>hm<\/jats:sup>than of pdk1<jats:sup>wt<\/jats:sup>mice. Similarly, proximal tubular electrogenic glucose transport in isolated, perfused renal tubule segments was decreased in pdk1<jats:sup>hm<\/jats:sup>compared with pdk1<jats:sup>wt<\/jats:sup>mice. Intraperitoneal injection of 3 g\/kg body wt glucose resulted in a similar increase of plasma glucose concentration in pdk1<jats:sup>hm<\/jats:sup>and in pdk1<jats:sup>wt<\/jats:sup>mice but led to a higher increase of urinary glucose excretion in pdk1<jats:sup>hm<\/jats:sup>mice. In conclusion, reduction of functional PDK-1 leads to impairment of electrogenic intestinal glucose absorption and renal glucose reabsorption. 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