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Published on: March 14, 2017
Acute Adaption to Oral or Intravenous Phosphate Requires Parathyroid Hormone
Linto Thomas1, Carla Bettoni1, Thomas Knöpfel1
1Institute of Physiology, University of Zurich, Zurich, Switzerland; and National Centre for Competence in Research, Zurich, Switzerland.
Phosphate loading rapidly increases urinary phosphate excretion (phosphaturia) via parathyroid hormone (PTH) and reduced renal phosphate transporters. The intestine does not stimulate renal clearance of phosphate.
Area of Science:
- Nephrology
- Endocrinology
- Mineral Metabolism
Background:
- Phosphate homeostasis involves complex renal, intestinal, and endocrine regulation.
- Early adaptive mechanisms and the intestine's role in phosphate regulation are not fully understood.
Purpose of the Study:
- To investigate the acute mineral, endocrine, and renal responses to phosphate loading.
- To elucidate the mechanisms of early phosphaturia and the intestine's role.
Main Methods:
- Intravenous and intragastric phosphate loading in rats.
- Measurement of plasma mineral, hormone levels, and creatinine clearance.
- Assessment of renal phosphate transporter expression and activity.
Main Results:
- Intravenous phosphate loading induced rapid phosphaturia, increased parathyroid hormone (PTH), and decreased renal phosphate transporter activity.
- Gastric phosphate loading showed delayed responses and did not alter plasma mineral levels.
- Phosphate-induced phosphaturia required PTH; the intestine did not stimulate renal phosphate clearance.
Conclusions:
- Acute phosphate loading triggers rapid phosphaturia through PTH-dependent mechanisms and downregulation of renal phosphate transporters.
- The intestine does not play a significant role in stimulating the renal clearance of phosphate during acute loading.
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