γ-Linolenic acid dietary supplementation can reverse the aging influence on rat liver microsome Δ6-desaturase activity

Abstract

We have recently demonstrated that in rats the process of Δ 6-desaturation of linoleic and α-linolenic acids slows with aging. One method of counteracting the effect of slowed desaturation of linoleic acid would be to provide the 6-desaturated metabolite, γ-linolenic acid (18:3( n−6) GLA) directly. We have here investigated the 6-desaturation of both linoleic and α-linolenic acids in liver microsomes of young and old rats given GLA in the form of evening primrose oil (EPO) (B diet) in comparison to animals given soy bean oil alone (A diet), monitoring also the fatty acid composition of liver microsomes and relating this to the microviscosity of the membranes. In young rats the different experimental diets did not produce any difference in Δ 6-desaturase (D6D) activity on either substrate suggesting that, when D6D activity is at or near its peak, the variations in diet tested are unable to influence it. In the old animals the rate of 6-desaturation of linoleic and particularly of α-linolenic acid was significantly greater in the B diet fed animals than in the A diet fed. The effects of the diets on the fatty acid composition of liver microsomes were consistent with the findings with regard to 6-desaturation. Administration of GLA partially corrected the abnormalities of n−6 essential fatty acid (EFA) metabolism by raising the concentration of 20:4( n−6) and other 6-desaturated EFAs. Furthermore, the GLA rich diet also increased the levels of dihomo-γ-linolenic acid and of 6-desaturated n−3 EFAs in the liver microsomes. The microviscosity of microsomal membranes as indicated by DPH polarization was correlated with the unsaturation index of the same membranes. There was a very strong correlation between the two. In both young and old rats the B diet reduced the microviscosity and increased the unsaturation index. However, the effect was much greater in the old animals.