Davis J W, Vanden Heuvel J P, Peterson R E
School of Pharmacy, University of Wisconsin, Madison 57306.
Lipids. 1991 Oct;26(10):857-9. doi: 10.1007/BF02536170.
Perfluorodecanoic acid (PFDA) is a peroxisome proliferator that causes a dose-dependent (20-80 mg/kg) increase in hepatic triacylglycerol and cholesteryl ester levels in the rat. We hypothesized that PFDA may cause an increase in the de novo synthesis of fatty acids and cholesterol in this species, which would explain observed effects. The incorporation of 3H2O into tissue lipids was examined 7 days after rats received vehicle or 20 or 80 mg/kg of PFDA. PFDA treatment decreased the rate of synthesis of cholesterol and fatty acids in the live and in epididymal fat pad. At a PFDA dose (20 mg/kg) that decreased de novo synthesis of fatty acids and cholesterol, there was no effect on the concentration of fatty acids and cholesterol in the liver, epididymal fat pads, and plasma. We conclude that PFDA induced fatty liver is due to either a decrease in the oxidation of fatty acids in the liver, or an impairment of triacylglycerol catabolism and/or export from the liver, and is not the result of an increase in de novo synthesis of fatty acids and cholesterol.
全氟癸酸（PFDA）是一种过氧化物酶体增殖剂，可使大鼠肝脏中的三酰甘油和胆固醇酯水平呈剂量依赖性（20 - 80毫克/千克）升高。我们推测PFDA可能会导致该物种脂肪酸和胆固醇的从头合成增加，这可以解释观察到的效应。在大鼠接受赋形剂或20或80毫克/千克PFDA 7天后，检测了3H2O掺入组织脂质的情况。PFDA处理降低了肝脏和附睾脂肪垫中胆固醇和脂肪酸的合成速率。在降低脂肪酸和胆固醇从头合成的PFDA剂量（20毫克/千克）下，对肝脏、附睾脂肪垫和血浆中的脂肪酸和胆固醇浓度没有影响。我们得出结论，PFDA诱导的脂肪肝是由于肝脏中脂肪酸氧化减少，或三酰甘油分解代谢和/或从肝脏输出受损，而不是脂肪酸和胆固醇从头合成增加的结果。
