Lack of correlation between the rate of cholesterol biosynthesis and the activity of 3-hydroxy-3-methylgutaryl coenzyme A reductase in rats and in fibroblasts treated with ML-236B.
Lack of correlation between the rate of cholesterol biosynthesis and the activity of 3-hydroxy-3-methylgutaryl coenzyme A reductase in rats and in fibroblasts treated with ML-236B.
复制标题
在用 ML-236B 处理的大鼠和成纤维细胞中，胆固醇生物合成速率与 3-羟基-3-甲基戊二酰辅酶 A 还原酶活性之间缺乏相关性。
DOI：
10.1016/0006-291x(78)90602-2
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发表时间：
1978
影响因子：
3.1
通讯作者：
E. Diller
中科院分区：
文献类型：
--
作者：
W. Bensch;T. Ingebritsen;E. Diller
ML-236 B是3-羟基-3-甲基戊二酰辅酶A还原酶的竞争性抑制剂，在大鼠和培养的人成纤维细胞中进行了研究。在进食和禁食大鼠中发现肝脏还原酶显著增加;对胆固醇-7 α-羟化酶无影响。ML-236 B未改变进食或禁食大鼠的组织固醇水平。在正常或家族性高胆固醇血症个体的成纤维细胞中，ML-236 B引起还原酶显著增加。相反，掺入甾醇的[2- 14 C]-乙酸减少，而掺入脂肪酸增加。放线菌酮阻止成纤维细胞还原酶的增加。
ML-236B, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was studied in the rat and cultured human fibroblasts. A marked increase in liver reductase was found in fed and fasted rats; there was no effect on cholesterol-7α-hydroxylase. ML-236B did not alter tissue sterol levels in fed or fasted rats. In fibroblasts from normal or familial hypercholesterolemic individuals, ML-236B caused a marked increase in reductase. In contrast, the incorporation [2-14C]-acetate into sterol was decreased while the incorporation into fatty acids was increased. Cycloheximide prevented the increase in fibroblast reductase.