Reproductive Biology and Endocrinology
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Klari Noormets1  , Sulev Kõks2,3  , Ants Kavak3 , Andres Arend4 , Marina Aunapuu4 , Aivi Keldrimaa1 , Eero Vasar2 and Vallo Tillmann1
1 Department of Paediatrics, University of Tartu, 6 Lunini Street, 51014 Tartu, Estonia
2 Department of Physiology, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
3 Institute of Veterinary Medicine and Animal Sciences, Estonian University of Life Sciences, 62 Kreutzwaldi Street, 51014 Tartu, Estonia
4 Department of Anatomy, Chair of Histology and Embryology, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
 author email corresponding author email
Reproductive Biology and Endocrinology 2009, 7:82doi:10.1186/1477-7827-7-82
The electronic version of this article is the complete one and can be found online at: http://www.rbej.com/content/7/1/82
| Received: |
19 March 2009 |
| Accepted: |
10 August 2009 |
| Published: |
10 August 2009 |
© 2009 Noormets et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
Wolfram Syndrome (WS) is an autosomal recessive disorder characterised by non-autoimmune diabetes mellitus, optic atrophy, cranial diabetes insipidus and sensorineural deafness. Some reports have described hypogonadism in male WS patients. The aim of our study was to find out whether Wfs1 deficient (Wfs1KO) male mice have reduced fertility and, if so, to examine possible causes.
Methods
Wfs1KO mice were generated by homologous recombination. Both Wfs1KO and wild type (wt) male mice were mated with wt female mice. The number of litters and the number of pups were counted and pregnancy rates calculated. The motility and morphology of the sperm and the histology of testes were analysed. Serum testosterone and FSH concentrations were also measured.
Results
The pregnancy rate in wt females mated with Wfs1KO males was significantly lower than in the control group (15% vs. 32%; p < 0.05), but there was no significant difference in litter size. Analysis of male fertility showed that, in the Wfs1KO group, eight males out of 13 had pups whereas in the control group all 13 males had at least one litter. Sperm motility was not affected in Wfs1KO mice, but Wfs1KO males had less proximal bent tails (14.4 +/- 1.2% vs. 21.5 +/- 1.3 p < 0.05) and less abnormal sperm heads (22.8 +/- 1.8 vs. 31.5 +/- 3.5, p < 0.05) than wt males. Testes histology revealed significantly reduced number of spermatogonia (23.9 +/- 4.9 vs. 38.1 +/- 2.8; p < 0.05) and Sertoli cells (6.4 +/- 0.5 vs. 9.2 +/- 1.0; p < 0.05) in Wfs1KO mice. Serum testosterone and FSH concentrations did not differ between the two groups.
Conclusion
The impaired fertility of Wfs1KO male mice is most likely due to changes in sperm morphology and reduced number of spermatogenic cells. The exact mechanism through which the Wfs1 gene influences sperm morphology needs to be clarified in further studies. | 
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