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[乙醇给药后大鼠高脂蛋白血症的发病机制]

[Pathogenesis of hyperlipoproteinemia in rats after the administration of ethanol].

作者信息

Titov V N, Pishchin D G

出版信息

Vopr Med Khim. 1978 Mar-Apr;24(2):244-52.

PMID:664451
Abstract

Single administration of ethanol at a dose of 6 g/kg of body weight caused accumulation of triglycerides in rat liver and development of hyperlipoproteinemia. Synthesis of mono-, di-, triglycerides and apoproteins of lipoproteins of very low density was increased in liver tissue. Lipoproteins of very low density were accumulated in blood; their transformation to lipoproteins of low density was impaired and synthesis of high density lipoproteins was decreased. In fatty tissue synthesis of fatty acids was decreased with simultaneous increase in activity of hormone-dependent lipoprotein lipase. Utilization of acetyl CoA pools, formed from exogenous 14C-acetate and 3H-leucine, was dissimilar in synthesis of neutral lipids and phospholipids; the phenomenon demonstrated that acetyl CoA pools were compartmentalized in synthesis of fatty acids.

摘要

以6克/千克体重的剂量单次给予乙醇会导致大鼠肝脏中甘油三酯的积累和高脂蛋白血症的发展。肝脏组织中极低密度脂蛋白的单甘油酯、二甘油酯、甘油三酯和载脂蛋白的合成增加。极低密度脂蛋白在血液中积累;它们向低密度脂蛋白的转化受损,高密度脂蛋白的合成减少。在脂肪组织中,脂肪酸的合成减少,同时激素依赖性脂蛋白脂肪酶的活性增加。由外源性14C-乙酸盐和3H-亮氨酸形成的乙酰辅酶A池在中性脂质和磷脂的合成中的利用情况不同;这一现象表明乙酰辅酶A池在脂肪酸合成中是分隔存在的。

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