| First Author | Blomberg Jensen M | Year | 2013 |
| Journal | Mol Cell Endocrinol | Volume | 377 |
| Issue | 1-2 | Pages | 93-102 |
| PubMed ID | 23850520 | Mgi Jnum | J:315508 |
| Mgi Id | MGI:6829110 | Doi | 10.1016/j.mce.2013.06.036 |
| Citation | Blomberg Jensen M, et al. (2013) Characterization of the testicular, epididymal and endocrine phenotypes in the Leuven Vdr-deficient mouse model: targeting estrogen signalling. Mol Cell Endocrinol 377(1-2):93-102 |
| abstractText | Vitamin D is a key factor for calcium and bone homeostasis, but signalling through the vitamin D receptor (VDR) seems also to be important for testicular function. To test the functional role of vitamin D signalling we examined the male reproductive system of the Leuven Vdr-ablated (Vdr(-/-)) mice, previously established as a model for hereditary vitamin D-resistant rickets. We investigated reproductive hormones, changes in gene expression and histological phenotype of eleven Vdr(-/-), eight Vdr(+/-) and nine Vdr(+/+) mice. Testicular and epididymal histology were grossly normal in Vdr(-/-) mice. Accordingly, no differences were found in serum concentrations of testosterone, estradiol, LH, and FSH or testicular expression of Cyp19a1, Ersalpha, Cyp17a1, Star, Insl3, Inhbb, and Amh. However, a significantly lower ERbeta expression was found in testis of Vdr(+/-) and Vdr(-/-) mice, conversely epididymal expressions of ERalpha and the estrogen-target gene Aqp9 were higher. In conclusion, vitamin D seems dispensable for murine spermatogenesis and sex hormone production, but aberrant estrogen-signalling may elicit some of the VDR-mediated effects on male reproduction. |
