AJP - Gastrointestinal and Liver Physiology, Vol 268, Issue 6 917-G924, Copyright © 1995 by American Physiological Society

ARTICLES

Sodium-phosphate transporter adaptation to dietary phosphate deprivation in normal and hypophosphatemic mice

J. F. Collins, N. Bulus and F. K. Ghishan
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2576, USA.

The X-linked hypophosphatemic (Hyp) mouse is a model for hypophosphatemic vitamin D-resistant rickets and is a homologue of human X-linked hypophosphatemia. The defect in the Hyp mouse appears to be related to decreased renal tubular reabsorption of P(i) via the renal brush-border membrane (Na(+)-P(i)) transporter. Dietary P(i) deprivation upregulates Na(+)-P(i) transport activity in brush-border membrane vesicles (BBMV) isolated from both normal and Hyp mice; however, the molecular mechanisms underlying this phenomenon are not known. The current studies were designed to investigate the effect of P(i) deprivation on the renal Na(+)-P(i) transporter. Low P(i) diet upregulated Na(+)-P(i) transporter activity in isolated BBMV by 2.1-fold in normal and Hyp mice (n = 3, P = 0.01). Low P(i) diet also induced a 1.9 +/- 0.3-fold increase in normal mice and 2.9 +/- 0.4-fold increase in Hyp mice in Na(+)-P(i) transporter message levels (n = 3, P = 0.028). The increase in message level encoding the Na(+)-P(i) transporter stimulated increased Na(+)-dependent P(i) uptake by Xenopus laevis oocytes when poly(A)+ RNA was injected into them from mice on low P(i) diet (approximately 1.67-fold in normal mice and 1.33-fold in Hyp mice). Immunoreactive protein levels increased 2.3 +/- 0.4-fold in normal mice and 8.2 +/- 0.5 in the Hyp mouse kidney cortexes (n = 3, P = 0.0001) in response to dietary P(i) deprivation.(ABSTRACT TRUNCATED AT 250 WORDS)

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