Vaartjes W J, De Haas C G, Haagsman H P
Biochem Pharmacol. 1986 Dec 1;35(23):4267-72. doi: 10.1016/0006-2952(86)90705-7.
In hepatocytes isolated from meal-fed rats, sodium 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA) decreased the rate of lipogenesis measured as incorporation of 3H from 3H2O into glycerolipids and cholesterol. Moreover, POCA inhibited the oxidation of added oleate, whereas oleate esterification was stimulated. In hepatocytes from 24-hr-starved rats, inhibition of gluconeogenesis by POCA was observed only with gluconeogenic precursors which require pyruvate carboxylation. This inhibition was secondary to impaired oxidation of long-chain fatty acids by POCA. It is concluded that, in addition to its inhibition of long-chain fatty acid oxidation, POCA interferes with de novo synthesis of cholesterol and fatty acids. On the other hand, neither fatty acid esterification nor the conversion of oxaloacetate into glucose are affected by POCA.
在从进食后大鼠分离出的肝细胞中,2-[5-(4-氯苯基)戊基]环氧乙烷-2-羧酸钠(POCA)降低了以3H2O中的3H掺入甘油脂质和胆固醇来衡量的脂肪生成速率。此外,POCA抑制添加油酸的氧化,而刺激油酸酯化。在饥饿24小时大鼠的肝细胞中,仅在需要丙酮酸羧化的糖异生前体存在时,才观察到POCA对糖异生的抑制作用。这种抑制是由于POCA损害长链脂肪酸氧化所致。得出的结论是,除了抑制长链脂肪酸氧化外,POCA还干扰胆固醇和脂肪酸的从头合成。另一方面,POCA既不影响脂肪酸酯化,也不影响草酰乙酸向葡萄糖的转化。