A sensitive radioreceptor assay for 1α,25‐dihydroxyvitamin D3 (1α,25‐(OH)2D3) is utilized to quantitate the circulating concentration of this sterol in experimental animals and humans. When weanling rats are grown for 2 weeks on low calcium or low phosphate diets, limited availability of either ion elicits a five‐fold increase in the plasma level of 1α,25‐(OH)2D3. The enhancement of 1α,25‐(OH)2D3 in calcium deficiency is dependent upon the presence of the parathyroid and/or thyroid glands, which is consistent with parathyroid hormone (PTH) mediation of this effect. In contrast, the response to phosphate deficiency is independent of these glands and may result from a direct action of low phosphate on the renal synthesis of 1α,25‐(OH)2D3. Studies in humans indicate that the normal level of 1α,25‐(OH)2D is 2.1‐4.5 ng/100 ml plasma. Patients with chronic renal failure have markedly lower circulating 1α,25‐(OH)2D and this kidney hormone is undectectable in anephirc subjects, but returns to normal within 1 day after successful renal transplantation. Hypoparathyroidism and pseudohypoparatghyroidism are associated with reduced plasma 1α,25‐(OH)2D while patients with primary hyperparathyroidism have significantly elevated sterol hormone levels. Thus, from measurements in rats and humans, it appears that circulating 1α,25‐(OH)2D3 is regulated by PTH and/or phosphate and that abnormal plasma 1α,25‐(OH)2D3 is a part of the pathophysiology of renal osteodystrophy and parathyroid disorders.
|Original language||English (US)|
|State||Published - Feb 1976|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism