Induction of fatty acid synthesis by pravastatin sodium in rat liver and primary hepatocytes
Induction of fatty acid synthesis by pravastatin sodium in rat liver and primary hepatocytes
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DOI：
10.1016/s0014-2999(97)83050-6
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发表时间：
1997-06-11
影响因子：
5
通讯作者：
Shimotsu, H
中科院分区：
文献类型：
--
作者：
Fujioka, T;Tsujita, Y;Shimotsu, H
我们研究了普伐他汀钠（普伐他汀），3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶抑制剂，对大鼠肝脏脂肪酸合成的影响。以250 mg/kg的剂量重复给予大鼠普伐他汀7天，导致肝脏中脂肪酸合成增加2.8倍。脂肪酸合成的日变化不受处理的影响。肝脂肪酸合成酶活性增加了3.2倍，而乙酰辅酶A羧化酶活性没有改变普伐他汀的重复给药。在大鼠肝细胞中，与2 μ g/ml普伐他汀孵育24小时增加脂肪酸合成酶活性1.5倍，以及HMG-CoA还原酶活性2.8倍。这些结果表明，HMG-CoA还原酶抑制剂可能通过诱导肝脂肪酸合成酶增加体内脂肪酸合成。(C)1997年Elsevier Science B.V.
We examined the effect of pravastatin sodium (pravastatin), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on fatty acid synthesis in rat liver. The repeated administration of pravastatin to rats at 250 mg/kg for 7 days led to a 2.8-fold increase in fatty acid synthesis in the liver. The diurnal change of fatty acid synthesis was not affected by the treatment. Hepatic fatty acid synthase activity was increased 3.2-fold, while acetyl-CoA carboxylase activity was not changed by the repeated administration of pravastatin. In rat hepatocytes, the incubation with 2 mu g/ml pravastatin for 24 h increased fatty acid synthase activity 1.5-fold, as well as HMG-CoA reductase activity 2.8-fold. These results suggest that HMG-CoA reductase inhibitors might increase fatty acid synthesis in vivo through the induction of hepatic fatty acid synthase. (C) 1997 Elsevier Science B.V.