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Submitted on December 9, 2005
Accepted on February 3, 2006
Laboratory of Clinical Chemistry, Faculty of Pharmacy, Katholieke Universiteit Leuven, Leuven, Belgium; Department of Medical Physiology, Division of Neurophysiology, University of Copenhagen, The Panum Institute, Copenhagen, Denmark; Laboratory for Experimental Medicine & Endocrinology, Department of Developmental Biology Katholieke Univesiteit Leuven, Leuven, Belgium; UMR 6175 INRA/CNRS/Université de Tours/Haras Nationaux, Physiologie de la Reproduction et des Comportements, Nouzilly, France; Department of Pharmacology, Faculty of Medicine, Katholieke Universiteit Leuven, Leuven, Belgium
* To whom correspondence should be addressed. E-mail: Myriam.Baes{at}pharm.kuleuven.be.
Inactivation of peroxisomal 
-oxidation in mice, by knocking-out multifunctional protein-2 (MFP-2, also called D-bifunctional enzyme), causes male infertility. In the testis extensive accumulations of neutral lipids were observed in Sertoli cells, beginning in prepubertal mice and evolving in complete testicular atrophy by the age of 4 months. Spermatogenesis was already severely affected at the age of 5 weeks and pre- and postmeiotic germ cells gradually disappeared from the tubuli seminiferi. Based on cytochemical stainings and biochemical analyses the lipid droplets consisted of cholesteryl esters and neutral glycerolipids. Furthermore, peroxisomal -oxidation substrates, such as very-long-chain fatty acids and pristanic acid accumulated in the testis, whereas the concentration of docosapentaenoic acid, a polyunsaturated fatty acid and peroxisomal -oxidation product, was reduced. The testicular defects were also present in double MFP-2/PPAR
knockout mice, ruling out the possibility that they were mediated through the activation of this nuclear receptor. Immunoreactivity for peroxisomal proteins, including MFP-2 was detected in Sertoli cells but also in germ cells and Leydig cells. The pivotal role of peroxisomal metabolism in Sertoli cells was further demonstrated by generating mice with a Sertoli cell selective elimination of peroxisomes, through cell type specific inactivation of the Pex5 gene. These mice also developed lipid inclusions, were infertile and their testes fully degenerated by the age of 4 months. In conclusion, the present data demonstrate that peroxisomal -oxidation is essential for lipid homeostasis in the testis and for male fertility.
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