LAUSR

Abstract It's considered that the amount of dietary saturated fatty acids (SFAs) intake is positively correlated with plasma cholesterol concentration. In mammals, de novo biosynthesis is the major resource of cholesterol, which could be promoted by SFAs. In this article, we discuss the probable mechanisms by which SFAs promote cholesterol synthesis. In human cells, the activation of sterol regulatory element-binding protein 2 pathway and degradation of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase elaborately regulate the synthesis by sensing cholesterol fluctuations in cells. SFAs lower intracellular cholesterol concentration via suppressing low density lipoprotein (LDL) endocytosis mediated by LDL receptor and retarding cholesterol transport from plasma membrane to endoplasmic reticulum.