Regulation of Hepatic Low-Density Lipoprotein Receptor, 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase, and Cholesterol 7α-Hydroxylase mRNAs in Human Liver
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چکیده
منابع مشابه
Macrophages Enhances Down-regulation of the Low Density Lipoprotein Receptor and 3-Hydroxy-3-methylglutaryl-Coenzyme A Reductase and Prevents Low Density Lipoprotein-induced Cholesterol Accumulation*
Cholesteryl ester accumulation in arterial wall macrophages (foam cells) is a prominent feature of atherosclerotic lesions. We have previously shown that 5774 macrophages accumulate large amounts of cholesteryl ester when incubated with unmodified low density lipoprotein (LDL) and that this is related to sluggish down-regulation of the 5774 LDL receptor and 3hydroxy-3-methylglutaryl-coenzyme A ...
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Rat liver microsomal 3-hydroxy-3-methylglutaric acid (HMG)-coenzyme A reductase (mevalonate:NADP oxidoreductase (acylating CoA), EC 1.1.1.34) exhibits a cyclic rhythm with peak activity at midnight. HMG-CoA reductase from microsomes of rats killed at noon and midnight has similar properties. Cycloheximide completely prevents the 5to IO-fold rise in activity which occurs from 6 p.m. to midnight,...
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The ability of mitogenic stimulation of human T lymphocytes to alter the expression of genes involved in sterol metabolism was examined. Messenger RNA levels for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, HMG-CoA synthase, and low density lipoprotein (LDL) receptor were quantified in resting and mitogen-stimulated T lymphocytes by nuclease protection assay. Mitogenic stimulation...
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Obesity is often associated with an elevated total body cholesterol synthesis. In order to evaluate the role of hepatic cholesterogenesis in this phenomenon, we assayed the rate-limiting step in cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase in the microsomal fraction of liver biopsies obtained operatively from ten morbidly obese (relative body weight greate...
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Treatment of rat intestinal epithelial cell cultures with the oxidosqualene cyclase inhibitor, 3 beta-[2-(diethylamino)-ethoxy]androst-5-en-17-one (U18666A), resulted in an accumulation of squalene 2,3:22,23-dioxide (SDO). When U18666A was withdrawn and the cells were treated with the sterol 14 alpha-demethylase inhibitor, ketoconazole, SDO was metabolized to a product identified as 24(S),25-ep...
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ژورنال
عنوان ژورنال: The Journal of Clinical Endocrinology & Metabolism
سال: 2002
ISSN: 0021-972X,1945-7197
DOI: 10.1210/jc.2002-012041