| Autor: |
Damir Zadravec, Petr Tvrdik, Hervé Guillou, Richard Haslam, Tsutomu Kobayashi, Johnathan A. Napier, Mario R. Capecchi, Anders Jacobsson |
| Jazyk: |
angličtina |
| Rok vydání: |
2011 |
| Předmět: |
|
| Zdroj: |
Journal of Lipid Research, Vol 52, Iss 2, Pp 245-255 (2011) |
| Druh dokumentu: |
article |
| ISSN: |
0022-2275 |
| DOI: |
10.1194/jlr.M011346 |
| Popis: |
ELOVL2 is a member of the mammalian microsomal ELOVL fatty acid enzyme family, involved in the elongation of very long-chain fatty acids including PUFAs required for various cellular functions in mammals. Here, we used ELOVL2-ablated (Elovl2−/−) mice to show that the PUFAs with 24–30 carbon atoms of the ω-6 family in testis are indispensable for normal sperm formation and fertility in male mice. The lack of Elovl2 was associated with a complete arrest of spermatogenesis, with seminiferous tubules displaying only spermatogonia and primary spermatocytes without further germinal cells. Furthermore, based on acyl-CoA profiling, heterozygous Elovl2+/− male mice exhibited haploinsufficiency, with reduced levels of C28:5 and C30:5n-6 PUFAs, which gave rise to impaired formation and function of haploid spermatides. These new insights reveal a novel mechanism involving ELOVL2-derived PUFAs in mammals and previously unrecognized roles for C28 and C30 n-6 PUFAs in male fertility. In accordance with the function suggested for ELOVL2, the Elovl2−/− mice show distorted levels of serum C20 and C22 PUFAs from both the n-3 and the n-6 series. However, dietary supplementation with C22:6n-3 could not restore male fertility to Elovl2+/− mice, suggesting that the changes in n-6 fatty acid composition seen in the testis of the Elovl2+/− mice, cannot be compensated by increased C22:6n-3 content. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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