Journal of Okayama Medical Association
Published by Okayama Medical Association

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血液細胞と肝の脂質代謝の比較に関する実験的研究 第2編 慢性四塩化炭素中毒による検討

河内 光男 岡山大学医学部第二内科
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抄録
In order to investigate the relationships between whole blood cells and liver slices on lipid metabolism in chronic CCl(4) intoxicated rats, the author studied in vitro incorporation of (14)C-acetate Na into gross lipid fracitons, major lipid fractions and total fatty acids. The results obtained are summarized as follows: 1) (14)C incorporation by liver slices into total lipids, unsaponifiable lipids and total fatty acids was markedly increased at 2 weeks, but at 12 weeks it was not so much increased except for total fatty acids than controls. On the other hand, (14)C incorporation by whole blood cells into each of them was similar to that obseved with controls at 2 weeks, while it was slightly decreased at 12 weeks. 2) Not only in acute CCl(4), intoxication but also in the chronic stage, as mentioned in Part I, it is considered that fatty liver would be caused by enhancement of TG and NEFA synthesis in liver, and at the same time lipid metabolism in whole blood cells would contribute to fatty liver. 3) An increae of percent (14)C incorporation by liver slices into fatty acid group 14:0+16:0, namely an increased acitivity of malonyl CoA pathway was observed at 2 weeks as well as at 12 weeks while whole blood cells incorporated relatively more radioactivity into fatty acid group 14:0+16:0 at 2 weeks, but at 12 weeks the percent radioactivity in oleic, 20 carbons' and more longer chains' fatty acids, derived from mitochondrial pathway, showed a significant relative increase. 4) As mentioned in Parts I and Ⅱ, lipid metabolism in liver slices was influenced strikingly following administration of CCl(4), but that in whole blood cells showed few differences between CCl(4) administered rats and controls. It may be possible to conclude from these results that whole blood cells would contribute to maintain the homeostasis of lipid metabolism in vivo.
備考
正誤表あり
ISSN
0030-1558
NCID
AN00032489