Most biological effects of zinc deficiency corrected by γ-linolenic acid (18: 3ω6) but not by linoleic acid (18: 2ω6)

Abstract

Zinc deficiency mimics many of the clinical features of essential fatty acid (EFA) deficiency in rats. Since zinc appears to be needed for the Δ-6-desaturase step in EFA metabolism, experiments were conducted to determine whether bypassing this step with γ-linolenic acid (18 : 3ω6) would alleviate the biological effects induced by a zinc-deficient diet. In pair-fed rats over a period of 5 weeks the deficient diet impaired growth and changed the relative weights of internal organs. It also induced hypolipidemia but had little effect on the fatty acid composition of tissue lipids. Daily subcutaneous injection of primrose oil containing 10% 18: 3ω6 reversed most of the effects of zinc deficiency on tissue weights, growth and plasma lipids. In contrast, injection of safflower oil, which has a similar content of linoleic acid (18 : 2ω6) but is devoid of 18 : 3ω6, had only a partial effect on some tissue weight changes. Neither oil affected the plasma fatty acid pattern, but both of them increased liver triglyceride concentrations. They also elevated the proportion of 18 : 2ω6 in liver, skin and epididymal fat. The latter effects were not observed in the absence of zinc deficiency. Supplementing the diet of EFA-deficient animals with an excess of zinc in their drinking water did not affect the typical tissue fatty-acid pattern of EFA deficiency. It is suggested that several of the manifestations of zinc deficiency are mediated by a relative state of EFA deficiency attributable, at least in part, to a reduced conversion of 18 : 2ω6 to 18 : 3ω6 resulting in an accumulation of 18 : 2ω6 in tissues. These findings are consistent with a role of zinc as a cofactor in the Δ-6-desaturase enzyme reaction. The suggested role of zinc in essential fatty acid metabolism may be of significance in understanding how essential fatty acids protect against cardiovascular disease in general.