1995 年 41 巻 2 号 p. 217-225
Sesamin is known as a specific inhibitor of Δ-desaturation, the conversion from dihoo-γ-linolenic acid (20: 3(n-6)) to arachidonic acid (20:4(n-6)). In the previous paper, we reported that sesamin inhibited Δ-desaturation of n-6 fatty acids in rat hepatocytes but not that of n-3 fatty acids, from 20: 4(n-3) to 20: 5(n-3). Then, we studied the effects of sesamin on Δ-desaturation of n-6 and n-3 fatty acids in vivo. Rats were fed two types of diets containing sesamin (0.5% w/w) for 4 weeks as follows: in experiment 1 (Exp. 1) γ-linolenic acid-rich diet and in experiment 2 (Exp. 2) a-linolenic acid-rich diet. The fatty acid composi-tion of liver lipids was compared to those of control groups without sesamin. In both Exps. 1 and 2, sesamin increased the liver weight and phospholipid contents in liver. In Exp. 2, sesamin increased n-6 fatty acids and decreased n-3 fatty acids even though the diet was rich in n-3 fatty acids. Sesamin enhanced the composition ratio of 20: 3(n-6) in both Exps. 1 and 2. Decrease of Δ-desaturation index of n-6 fatty acid, the ratio of 20:4(n-6)/20: 3(n-6), by the administration of sesamin suggested that sesamin inhibited the Δ-desaturation of n-6 fatty acids in the liver. On the contrary, the Δ-desaturation index of n- 3 fatty acids, the ratio of 20: 5(n-3) to 18: 3(n-3), was increased by sesamin administration in the liver of rats fed a-linolenic acid-rich diet (Exp. 2). These results sug-gested that sesamin inhibited the Δ-desaturation of n-6 fatty acids but not that of n-3 fatty acids in vivo similarly to results from rat hepatocytes.
