肝障害時の脂質代謝に関する研究 第2編 四塩化炭素障害ラット肝におけるリノール酸およびγ-リノレン酸のアラキドン酸生成効果および脂肪肝抑制作用について

Gaschromatographic observatons of the quantities and the compositions of fatty acids in liver tissues were carried out of rats injured by carbon tetrachloride after feeding on free fat diet to investigate the effects of ethyl-linoleate administration with and without 29.6% γ-linolenate on injured liver. The results were as follows: 1. Arachidonate in phospholipid fraction of the control group increased two days after linoleate or γ-linolenate administrations. After eleven days this increased level of arachidonate was corresponded to two and three times of the control value respectively. Whereas in the carbon tetrachloride injected rats no increased synthesis of arachidonate could be observed two days after that treatment. Two fold increased synthesis of arachidonate was found, however, eleven days after the carbon tetrachloride treatment in the group with the linoleate or the γ-linolenate, and there were no differences in the both groups. 2. Palmitoleate and oleate in triglyceride fraction and cholesterolester fraction increased markedly at the regenerating stage in injured livers rather than the sever damaged stage. Other endogenous fatty acids as well as these fatty acids decreased below 50% by administration of these highly unsaturated fatty acids. 3. Fatty acid in phospholipid fraction was found to be about equal quantity in each group. On the other hand, in unsaturated fatty acids treated group, palmitoleate and oleate decreased with the simultaneous increase of linoleate and arachidonate. 4. Fatty acid in tryglyceride fraction, fatty acid in cholesterolester fraction and total fatty acid increased more remarked in the carbon tetrachloride treated group. These levels were decreased, however, 50% by the administration of highly unsaturated fatty acids, and such administration markedly inhibited the increase of these fatty acids. 5. From these findings the preventive effects of linoleate and γ-linolenate on carbon tetrachloride induced fatty liver might be explained as that the intrahepatic increase of administrated these fatty acids depressed the inflow of FFA into the liver tissues from peripheral fat tissues and the sequential synthesis of arachidonate accelerated the synthesis and secretion of lipoproteins.