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• W1963541108 abstract "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." @default.
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• W1963541108 date "2009-11-01" @default.
• W1963541108 modified "2023-10-14" @default.
• W1963541108 title "Regulation of rat intestinal Na-dependent phosphate transporters by dietary phosphate" @default.
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• W1963541108 doi "https://doi.org/10.1152/ajprenal.00279.2009" @default.
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