Cholesterol feeding reduces nuclear forms of sterol regulatory element binding proteins in hamster liver

摘要: Cholesterol feeding reduces the mRNAs encoding multiple enzymes in cholesterol biosynthetic pathway and low density lipoprotein receptor livers of hamsters. Here we show that also levels nuclear NH2-terminal domains sterol regulatory element binding proteins (SREBPs), which activate transcription sterol-regulated genes. We hamsters, like those mice humans, predominantly produce SREBP-2 1c isoform SREBP-1. Both are produced as membrane-bound precursors must be proteolyzed to release transcriptionally active domains. Diets containing 0.1% 1.0% decreased amount SREBP-1c without affecting membrane precursor or its mRNA, suggesting inhibits proteolytic processing SREBP-1 liver it does cultured cells. appeared reduce SREBP-2. In addition, at high dietary mRNA declined fell, accumulation may inhibit gene. The high-cholesterol diets reduced by 30% a more profound 70–90% reduction 3-hydroxy-3-methylglutaryl CoA synthase reductase. Treatment with lovastatin Colestipol, increases hepatic demands for cholesterol, increased well forms protein. This treatment caused reciprocal decline Considered together, these data suggest SREBPs play important roles controlling genes liver, they do