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WATER AND ELECTROLYTE HOMEOSTASIS

Impaired intestinal and renal glucose transport in PDK-1 hypomorphic mice

¹Department of Physiology I, University of Tübingen, Tübingen, Germany; ²Department of Physiology, Innsbruck Medical University, Innsbruck, Austria; ³Institute of Physiology and Center for Integrative Human Physiology, University of Zürich, Zürich, Switzerland; and ⁴Department of Biochemistry, University of Dundee, Dundee, United Kingdom

Submitted 11 January 2006 ; accepted in final form 30 May 2006

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⁺-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 20% of PDK-1 (pdk1^hm) were compared with their wild-type littermates (pdk1^wt). According to Ussing chamber experiments, electrogenic glucose transport was significantly smaller in the jejunum of pdk1^hm than of pdk1^wt mice. Similarly, proximal tubular electrogenic glucose transport in isolated, perfused renal tubule segments was decreased in pdk1^hm compared with pdk1^wt mice. Intraperitoneal injection of 3 g/kg body wt glucose resulted in a similar increase of plasma glucose concentration in pdk1^hm and in pdk1^wt mice but led to a higher increase of urinary glucose excretion in pdk1^hm mice. In conclusion, reduction of functional PDK-1 leads to impairment of electrogenic intestinal glucose absorption and renal glucose reabsorption. The experiments disclose a novel element of glucose transport regulation in kidney and small intestine.

glucosuria; insulin; sodium-dependent glucose transporter 1; phosphatidylinositol-3 kinase; growth factors; intestinal glucose transport

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