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MUCOSAL BIOLOGY

Regulation of Intestinal Phosphate Transport II. Metabolic acidosis stimulates Na⁺-dependent phosphate absorption and expression of the Na⁺-P_i cotransporter NaPi-IIb in small intestine

Institute of Physiology, University of Zurich, Zurich, Switzerland

Submitted 16 April 2004 ; accepted in final form 21 October 2004

During metabolic acidosis, P_i serves as an important buffer to remove protons from the body. P_i is released from bone together with carbonate buffering protons in blood. In addition, in the kidney, the fractional excretion of phosphate is increased allowing for the excretion of more acid equivalents in urine. The role of intestinal P_i absorption in providing P_i to buffer protons and compensating for loss from bone during metabolic acidosis has not been clarified yet. Inducing metabolic acidosis (NH₄Cl in drinking water) for 2 or 7 days in mice increased urinary fractional P_i excretion twofold, whereas serum P_i levels were not altered. Na⁺-dependent P_i transport in the small intestine, however, was stimulated from 1.89 ± 3.22 to 40.72 ± 11.98 pmol/mg protein (2 days of NH₄Cl) in brush-border membrane vesicles prepared from total small intestine. Similarly, the protein abundance of the Na⁺-dependent phosphate cotransporter NaPi-IIb in the brush-border membrane was increased 5.3-fold, whereas mRNA levels remained stable. According to immunohistochemistry and real-time PCR NaPi-IIb expression was found to be mainly confined to the ileum in the small intestine, and this distribution was not altered during metabolic acidosis. These results suggest that the stimulation of intestinal P_i absorption during metabolic acidosis may contribute to the buffering of acid equivalents by providing phosphate and may also help to prevent excessive liberation of phosphate from bone.

phosphate

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