Journal of Nutrition

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


Journal of Nutrition Vol. 122 No. 6 June 1992, pp. 1338-1344
Copyright © 1992 by American Society for Nutrition
This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Uhland, A. M.
Right arrow Articles by DeLuca, H. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Uhland, A. M.
Right arrow Articles by DeLuca, H. F.

Normalization of Serum Calcium Restores Fertility in Vitamin D-Deficient Male Rats1,2,

Ann M. Uhland, Gary G. Kwiecinski3 and Hector F. DeLuca4

Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, Madison, WI 53706

We performed experiments to determine whether treatment with vitamin D or 1,25-dihydroxycholecalciferol could reverse male infertility caused by vitamin D deficiency. Additionally, an attempt was made to distinguish between a direct and an indirect effect of 1,25-dihydroxycholecalciferol on reproductive tissue. Vitamin D-deficient male rats with impaired fertility were treated with vitamin D and 1,25-dihydroxycholecalciferol for 3 wk, then mated. Secondly, vitamin D-deficient male rats were made normocalcemic by increasing dietary calcium, and their fertility was compared with that of vitamin D-deficient, hypocalcemic rats. The fertility of male rats was restored by treatment with either vitamin D or 1,25-dihydroxycholecalciferol. However, fertility was also restored in vitamin D-deficient animals by feeding them a diet supplemented with high levels of calcium. These results indicate that the influence of vitamin D and its active metabolite, 1,25-dihydroxycholecalciferol, on male fertility is indirect. Vitamin D and 1,25-dihydroxycholecalciferol seemed to influence male fertility by acting on classic target tissues and regulating levels of calcium in reproductive tissues.


KEY WORDS: • vitamin D deficiency • male fertility • reproduction • rats • calcium

1 This work was supported in part by a Program Project Grant no. DK-14881 from the National Institutes of Health and by the Harry Steenbock Research Fund of the Wisconsin Alumni Research Foundation.

2 Reprints are not available.

3 Current address: Department of Biology, University of Scranton, Scranton, PA 18510.

4 To whom correspondence should be addressed.

Manuscript received 29 August 1991. Revision accepted 13 January 1992.




This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
G.-S. Lee, K.-C. Choi, and E.-B. Jeung
Glucocorticoids differentially regulate expression of duodenal and renal calbindin-D9k through glucocorticoid receptor-mediated pathway in mouse model
Am J Physiol Endocrinol Metab, February 1, 2006; 290(2): E299 - E307.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]