| 19675183 |
Giral H, Caldas Y, Sutherland E, Wilson P, Breusegem S, Barry N, Blaine J, Jiang T, Wang XX, Levi M: Regulation of rat intestinal Na-dependent phosphate transporters by dietary phosphate. Am J Physiol Renal Physiol. 2009 Nov;297(5):F1466-75. Epub 2009 Aug 12.
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. |
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