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Essential fatty acid deficiency induces fatty acid desaturase expression in rat epididymis, but not in testis

¹ Andrology Laboratory, Departments of Gynecology and Obstetrics,² Medical Biochemistry, Rikshospitalet University Hospital, N-0027 Oslo, Norway,³ Institute of Clinical Biochemistry, Faculty Division Rikshospitalet,⁴ Department of Nutrition, Institute of Basic Medical Sciences,⁵ Department of Molecular Biosciences, University of Oslo, N-0316 Oslo, Norway and⁶ Faculty of Health Sciences, Oslo University College, N-0130 Oslo, Norway

Correspondence should be addressed to T B Haugen, Faculty of Health Sciences, Oslo University College, PO Box 4, St Olavs plass, N-0130 Oslo, Norway; Email: trine.b.haugen{at}hf.hio.no

On the molecular level, essential fatty acid deficiency (EFAD) has been associated with induced fatty acid (FA) desaturase expression and activity in several tissues. However, there seem to be exceptions. In the present study, we examine the effects of EFAD in the male rat genital tract, combining FA analysis, gene expression studies, and morphological evaluation of epididymal spermatozoa. When feeding 21-day-old Wistar rats, a fat-free diet for 6 weeks, an increase in 18:1n-9 and 20:3n-9 and a concomitant decrease in the 18:2n-6 and 20:4n-6 species are seen in testis, as well as in liver. However, with regard to desaturase expression the rat testis seems to be unresponsive to EFAD conditions, in contrast to other organs studied. In the sexually mature testis none of the desaturases (SCD1, SCD2, D5D, or D6D) are induced in response to lowered contents of polyunsaturated FAs. This also applies to caput epididymis, while EFAD sensitivity is regained in cauda epididymis, where the desaturases are upregulated. The FA profile of epididymal spermatozoa is increasingly affected by EFAD during the transport from testis to cauda epididymis. Furthermore, a significant increase in the number of abnormal spermatozoa is observed in cauda epididymis.