Sesamin is a specific inhibitor of Δ5 desaturation, the conversion from dihomo-γ-linolenic acid (20 : 3, n-6) to arachidonic acid (AA, 20 : 4, n-6). Previously, we reported that sesamin inhibited Δ5 desaturation of n-6 fatty acids in rat hepatocytes but not that of n-3 fatty acids, from 20 : 4 (n-3) to eicosapentaenoic acid (EPA, 20 : 5, n-3). In this study, we investigated the interaction of sesamin and EPA on Δ5 desaturation of both series and the n-6/n-3 fatty acids ratio by measuring actural fatty acid contents in vivo. Rats were fed three types of dietary oils ; 1) linoleic acid (LA, 18 : 2, n-6) : linolenic acid (LLA, 18 : 3, n-3) =3 : 1, n-6/n-3 ratio of 3 : 1 (LA group), 2) LA : LLA = 1 : 3, n-6/n-3 ratio of 1 : 3 (LLA group), 3)LA : LLA : EPA = 1 : 0. 5 : 3, n-6/n-3 ratio of 1 : 3. 5 (EPA group) with or without sesamin (0. 5% w/w) for 4 weeks. In all groups, sesamin administration increased the content of dihomo-γ-linolenic acid (20 : 3, n-6)in the liver and decreased the A5 desaturation index of n-6 fatty acid, the ratio of 20 : 4/20 : 3 (n-6). On the contrary, the Δ5 desaturation index of n-3 fatty acid, the ratio of 20 : 5 + 22 : 5 + 22 : 6/20 : 4 (n-3), was increased by the administration of sesamin. These results suggest that sesamin inhibits the Δ5 desaturation of n-6 fatty acid, but not that of n-3 fatty acid in rat livers. Sesamin administration decreased incorporation of EPA (n-3) and simultaneously increased the AA (n-6) content in the liver. The n-6/n-3 ratio in the liver was increased by administering sesamin under n-3 rich conditions, i.e., the LLA and EPA groups.

This article cannot obtain the latest cited-by information.