Abnormal hyperphosphatemic response to fasting in X-linked hypophosphatemic mice.
It has been proposed that renal inorganic phosphate (Pi) transport adaptation is a prerequisite for the hyperphosphatemic effect of fasting in animals previously fed low Pi diet (LPD). To test the validity of this proposal we have used X-linked hypophosphatemic (HYP) mice, since these animals are unable to adapt their renal Pi transport to LPD. HYP and control mice were pair-fed either high Pi diet (HPD) or LPD for 9 days. Then the influence of 24-hour fasting on plasma and urine Pi was studied. In the HPD condition, fasting led to a decrease in plasma Pi concentration, [Pi]P1, in both control and HYP mice. In the LPD condition fasting markedly increased [Pi]P1 from 1.61 +/- 0.13 mmol/l (mean +/- SEM, n = 8) to 2.33 +/- 0.05 mmol/l (n = 8, p less than 0.001) in control mice. In sharp contrast, in HYP mice fed LPD [Pi]P1 tended to decrease from 1.17 +/- 0.10 (n = 7) to 0.91 +/- 0.12 mmol/l (n = 7). As estimated from 24-hour urinary Pi excretion the mobilization of Pi from body stores was not different in HYP as compared to control mice fed either LPD or HPD. In conclusion, the results of this study support the hypothesis that the renal Pi transport adaptation to dietary Pi restriction is indeed the prerequisite for a hyperphosphatemic response to fasting. They also suggest that the mobilization of Pi from body stores during fasting with LPD is normal in HYP mice, even after Pi restriction.
D000818:Animals; D001692:Biological Transport; D005215:Fasting; D005260:Female; D007015:Hypophosphatemia, Familial / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010710:Phosphates / Q000097:blood*
D010710:Phosphates