Effects of linoleate and arachidonate deficiencies on reproduction and spermatogenesis in the cat

The inability of the cat to convert significant quantities of linoleate [18:2(9,12)] to arachidonate [20:4(5,8,11,14]) in the liver makes the cat a useful model for studying the specific physiological roles of these two fatty acids. In these studies, cats were fed purified diets that were either deficient in essential fatty acids (EFAs) or that provided linoleate with or without arachidonate. Male cats that were fed the EFA-deficient diet for approximately 2 years exhibited extensive degeneration of the testes, and the fatty acid composition of testes changed in a manner consistent with EFA deficiency. Linoleate prevented testis degeneration. Levels of arachidonate, 22:4n6, and 22:5n6 were higher in testis phospholipids of cats supplied with linoleate than in the deficient cats, indicating that the testis of the cat has the capacity to desaturate and elongate linoleate. In contrast, female cats that were fed diets lacking arachidonate were unable to bear live kittens, whether linoleate was provided in the diet or not. Arachidonate, supplied by oral supplements of ethyl arachidonate or by animal fat in the diet, significantly improved reproduction. Thus, linoleate appears to meet the requirements for spermatogenesis in males, but dietary arachidonate is essential for adequate reproduction in female cats.