Secondary hyperparathyroidism and phosphate sensing in parathyroid glands

J Med Invest. 2000 Aug;47(3-4):118-22.

Abstract

Retention of inorganic phosphate (Pi) and associated hyperphosphatemia are important development of hyperparathyroidism secondary to renal failure. The beneficial effect of a low-Pi diet in the prevention of hyperparathyroidism can be attributed to the decrease in PTH secretion. This effect of Pi may be mediated by specific molecules in the parathyroid cell membrane. A complementary DNA encoding a Na(+)-Pi co-transporter, termed rat PiT-1, has been isolated from rat parathyroid. The amount of PiT-1 mRNA in the parathyroid is controlled by vitamin D and dietary Pi, which are the most important regulators of PTH secretion. The parathyroid Pi transporter may mediate the effects of extracellular Pi and PTH secretion in secondary hyperparathyroidism. In this study, we focus on the function of Na/Pi co-transporters in the parathyroid glands as inorganic Pi sensor.

MeSH terms

  • Animals
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cloning, Molecular
  • Gene Expression Regulation
  • Hyperparathyroidism / metabolism*
  • Hyperparathyroidism / physiopathology
  • Parathyroid Glands / metabolism*
  • Parathyroid Glands / physiopathology
  • Phosphates / metabolism*
  • Rats
  • Sodium-Phosphate Cotransporter Proteins
  • Sodium-Phosphate Cotransporter Proteins, Type III
  • Symporters*
  • Vitamin D / metabolism

Substances

  • Carrier Proteins
  • Phosphates
  • Slc20a1 protein, rat
  • Sodium-Phosphate Cotransporter Proteins
  • Sodium-Phosphate Cotransporter Proteins, Type III
  • Symporters
  • Vitamin D