Barak A J, Sorrell M F, Tuma D J
Lipids. 1979 Nov;14(11):883-7. doi: 10.1007/BF02533500.
Total lipoproteins as well as fractionated VLDL + LDL and HDL from fasted control rats and bile-ligated rats were tested in liver perfusion for their effect on 3-hydroxy-3-methylglutaryl CoA reductase activity in normal rat livers. The total lipoproteins of bile-obstructed rats had 3 times greater capacity to increase 3-hydroxy-3-methylglutaryl CoA reductase activity than that of the control total lipoproteins. When the fractionated lipoproteins were tested from fasted control rats, it was found that the major stimulating activity was in the HDL fraction with minor activity in the VLDL + LDL fraction. When these plasma components isolated from fasted bile-ligated rats were tested, it was found that the major activity had shifted to the VLDL + LDL fraction with the HDL having only a minor stimulatory role. The possible mechanism of action of the abnormal lipoproteins associated with bile obstruction in regulating 3-hydroxy-3-methylglutaryl CoA reductase activity is discussed.
对禁食的对照大鼠和胆管结扎大鼠的总脂蛋白以及分级分离的极低密度脂蛋白(VLDL)+低密度脂蛋白(LDL)和高密度脂蛋白(HDL)进行肝脏灌注试验,以研究它们对正常大鼠肝脏中3-羟基-3-甲基戊二酰辅酶A还原酶活性的影响。胆管梗阻大鼠的总脂蛋白增加3-羟基-3-甲基戊二酰辅酶A还原酶活性的能力是对照总脂蛋白的3倍。对禁食对照大鼠分级分离的脂蛋白进行检测时,发现主要的刺激活性存在于HDL组分中,而VLDL + LDL组分中的活性较小。当检测从禁食胆管结扎大鼠分离的这些血浆成分时,发现主要活性已转移至VLDL + LDL组分,而HDL仅具有较小的刺激作用。文中讨论了与胆管梗阻相关的异常脂蛋白调节3-羟基-3-甲基戊二酰辅酶A还原酶活性的可能作用机制。