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This Article Full Text Full Text (PDF) Supplemental Figures and Tables All Versions of this Article: 297/5/F1466    most recent 00279.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Giral, H. Articles by Levi, M. PubMed PubMed Citation Articles by Giral, H. Articles by Levi, M.

Regulation of rat intestinal Na-dependent phosphate transporters by dietary phosphate

Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver, and Veterans Affairs Medical Center, Aurora, Colorado

Submitted May 21, 2009 ; accepted in final form August 6, 2009

Hyperphosphatemia associated with chronic kidney disease is one of the factors that can promote vascular calcification, and intestinal P_i absorption is one of the pharmacological targets that prevents it. The type II Na-P_i cotransporter NaPi-2b is the major transporter that mediates P_i reabsorption in the intestine. The potential role and regulation of other Na-P_i transporters remain unknown. We have identified expression of the type III Na-P_i cotransporter PiT-1 in the apical membrane of enterocytes. Na-P_i transport activity and NaPi-2b and PiT-1 proteins are mostly expressed in the duodenum and jejunum of rat small intestine; their expression is negligible in the ileum. In response to a chronic low-P_i diet, there is an adaptive response restricted to the jejunum, with increased brush border membrane (BBM) Na-P_i transport activity and NaPi-2b, but not PiT-1, protein and mRNA abundance. However, in rats acutely switched from a low- to a high-P_i diet, there is an increase in BBM Na-P_i transport activity in the duodenum that is associated with an increase in BBM NaPi-2b protein abundance. Acute adaptive upregulation is restricted to the duodenum and induces an increase in serum P_i that produces a transient postprandial hyperphosphatemia. Our study, therefore, indicates that Na-P_i transport activity and NaPi-2b protein expression are differentially regulated in the duodenum vs. the jejunum and that postprandial upregulation of NaPi-2b could be a potential target for treatment of hyperphosphatemia.

SLC34A2; PiT-1; hyperphosphatemia; chronic kidney disease; dietary P_i