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The Mechanism of the Action of Growth Hormone on Vitamin D Metabolism in the Rat

The Mechanism of the Action of Growth Hormone on Vitamin D Metabolism in the Rat GH has been shown to stimulate intestinal calcium absorption in rats and humans. We have investigated in rats whether GH might affect intestinal calcium absorption by stimulating the production of 1,25-dihydroxyvitamin D3 [1,25- (OH)2D3], the active metabolite of vitamin D3. The tissue distribution of [3H]1,25-(OH)2D3 8–40 h after iv injection of [3H]25-hydroxyvitamin D3 ([3H]25OHD3) was measured in sham controls, hypophysectomized, and GH-treated hypophysectomized rats. Since the plasma disappearance rate of iv [3H]1,25-(OH)2D3 was not significantly affected by hypophysectomy, the recovery of [3H]1,25-(OH)2D3 after [3H]25OHD3 administration was taken to be an indirect measure of renal 25- OHD3-l-hydroxylase. Hypophysectomy was found to reduce the recovery of [3H]1,25-(OH)2D3 from serum and intestinal mucosa by 70 ± 2% (range). A 6-day course of GH treatment of hypophysectomized rats restored the formation of 1,25-(OH)2D3 to normal, and a significant effect was noted within 2 days, before any increase in renal weight was detectable. No other pituitary hormones appeared to be necessary. The markedly atrophic intestinal mucosa of hypophysectomized rats incorporated iv [3H]1,25-(OH)2D3 normally. However, it remains to be determined whether 1,25-(OH)2D3 alone can correct the decreased calcium transport in hypophysectomized rats. (Endocrinology108: 1064, 1981) This content is only available as a PDF. Author notes * This work was supported by grants from Eli Lilly and Co., Indianapolis, IN, and the University of California, San Francisco, CA. This work was presented in part at the III Workshop on Vitamin D, Asilomar, CA, 1977, an abstract of which has been published (8). † Present address: School of Dentistry, University of California, San Francisco, CA 94143 Copyright © 1981 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Endocrinology Oxford University Press

The Mechanism of the Action of Growth Hormone on Vitamin D Metabolism in the Rat

Endocrinology , Volume 108 (3) – Mar 1, 1981

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References (20)

Publisher
Oxford University Press
Copyright
Copyright © 1981 by The Endocrine Society
ISSN
0013-7227
eISSN
1945-7170
DOI
10.1210/endo-108-3-1064
Publisher site
See Article on Publisher Site

Abstract

GH has been shown to stimulate intestinal calcium absorption in rats and humans. We have investigated in rats whether GH might affect intestinal calcium absorption by stimulating the production of 1,25-dihydroxyvitamin D3 [1,25- (OH)2D3], the active metabolite of vitamin D3. The tissue distribution of [3H]1,25-(OH)2D3 8–40 h after iv injection of [3H]25-hydroxyvitamin D3 ([3H]25OHD3) was measured in sham controls, hypophysectomized, and GH-treated hypophysectomized rats. Since the plasma disappearance rate of iv [3H]1,25-(OH)2D3 was not significantly affected by hypophysectomy, the recovery of [3H]1,25-(OH)2D3 after [3H]25OHD3 administration was taken to be an indirect measure of renal 25- OHD3-l-hydroxylase. Hypophysectomy was found to reduce the recovery of [3H]1,25-(OH)2D3 from serum and intestinal mucosa by 70 ± 2% (range). A 6-day course of GH treatment of hypophysectomized rats restored the formation of 1,25-(OH)2D3 to normal, and a significant effect was noted within 2 days, before any increase in renal weight was detectable. No other pituitary hormones appeared to be necessary. The markedly atrophic intestinal mucosa of hypophysectomized rats incorporated iv [3H]1,25-(OH)2D3 normally. However, it remains to be determined whether 1,25-(OH)2D3 alone can correct the decreased calcium transport in hypophysectomized rats. (Endocrinology108: 1064, 1981) This content is only available as a PDF. Author notes * This work was supported by grants from Eli Lilly and Co., Indianapolis, IN, and the University of California, San Francisco, CA. This work was presented in part at the III Workshop on Vitamin D, Asilomar, CA, 1977, an abstract of which has been published (8). † Present address: School of Dentistry, University of California, San Francisco, CA 94143 Copyright © 1981 by The Endocrine Society

Journal

EndocrinologyOxford University Press

Published: Mar 1, 1981

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