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Decreased mRNA expression of the PTH/PTHrP receptor and type II sodium-dependent phosphate transporter in the kidney

Shin-ichi Katsumata1, Ritsuko Masuyama, Mariko Uehara

  • 1Department of Nutritional Science, Faculty of Applied Bioscience, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo 156-8502, Japan.

Bioscience, Biotechnology, and Biochemistry
|December 25, 2004
PubMed

Insights

High phosphorus diets disrupt parathyroid hormone (PTH) action in rat kidneys. This leads to suppressed PTH signaling and altered phosphate (P) excretion, impacting mineral homeostasis.

Area of Science:

  • Nephrology
  • Endocrinology
  • Mineral Metabolism

Background:

  • Dietary phosphorus (P) intake is crucial for mineral homeostasis.
  • Parathyroid hormone (PTH) regulates calcium and P levels.
  • Kidney plays a key role in P excretion and PTH action.

Purpose of the Study:

  • To investigate phosphorus homeostasis under altered parathyroid hormone (PTH) action.
  • To examine the effects of high P diets on kidney function and mineral balance in rats.

Main Methods:

  • Rats were fed diets with varying P levels (0.3% to 1.5%) for 21 days.
  • Serum P, calcium (Ca), PTH, and 1,25(OH)(2)D(3) levels were measured.
  • Urinary P excretion, cAMP, and kidney gene expression (PTH/PTHrP receptor, NaPi-2) were analyzed.

Main Results:

  • High P diets increased serum PTH and urinary P excretion.
  • Serum Ca decreased with P diets ≥1.2%, while 1,25(OH)(2)D(3) levels were initially elevated then unchanged.
  • Kidney PTH/PTHrP receptor and NaPi-2 mRNA expression decreased with high P diets (≥1.2%).

Conclusions:

  • High P diets suppress PTH action in the kidney via PTH/PTHrP receptor downregulation.
  • Increased urinary P excretion may result from decreased NaPi-2 mRNA, independent of PTH and 1,25(OH)(2)D(3).
  • Altered P intake significantly impacts renal P handling and PTH signaling pathways.

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