Ueno K, Hayashi H, Moriuchi A, Okuyama H
Biochim Biophys Acta. 1985 Nov 14;837(2):173-80.
A high cholesterol diet induced a fatty liver and an increase in cholesterol oleate in spontaneously hypertensive rats. The activity of microsomal glycerophosphate acyltransferase in liver increased 2-3-fold to meet the increased supply of oleate, the synthesis of which was stimulated by a 10-fold increase in microsomal delta 9-desaturase activity. Hepatic fatty acid synthetase and diacylglycerol acyltransferase activities were decreased somewhat. These results, together with the fact that the large increases in hepatic cholesterol ester and triacylglycerol were not correspondingly reflected in plasma, indicated that the fatty liver resulted from decreased secretion of lipoprotein rather than increased lipogenesis. Endogenous cholesterol in liver microsomes increased 2-fold and hepatic acyl-CoA:cholesterol acyltransferase activity increased 3-fold, whereas plasma lecithin:cholesterol acyltransferase activity was unchanged. Thus, the increase in cholesterol oleate seen in spontaneously hypertensive rats fed a high cholesterol diet is due mainly to increases in acyl-CoA:cholesterol acyltransferase and delta 9-desaturase activities.
高胆固醇饮食可导致自发性高血压大鼠出现脂肪肝，并使胆固醇油酸酯增加。肝脏微粒体甘油磷酸酰基转移酶的活性增加了2至3倍，以满足增加的油酸供应，而油酸的合成受到微粒体δ9-去饱和酶活性增加10倍的刺激。肝脏脂肪酸合成酶和二酰甘油酰基转移酶的活性略有下降。这些结果，连同肝脏胆固醇酯和三酰甘油大幅增加但未相应反映在血浆中的事实，表明脂肪肝是由于脂蛋白分泌减少而非脂肪生成增加所致。肝脏微粒体中的内源性胆固醇增加了2倍，肝脏酰基辅酶A：胆固醇酰基转移酶活性增加了3倍，而血浆卵磷脂：胆固醇酰基转移酶活性未变。因此，喂食高胆固醇饮食的自发性高血压大鼠中所见的胆固醇油酸酯增加主要是由于酰基辅酶A：胆固醇酰基转移酶和δ9-去饱和酶活性增加所致。
