Scavenger Receptor B-1 Emerges as Anti-atherogenic Candidate Scott M. Grundy  Cell Metabolism  Volume 23, Issue 5, Pages 755-757 (May 2016) DOI: 10.1016/j.cmet.2016.04.019 Copyright © 2016 Terms and Conditions

Figure 1 Reverse Cholesterol Transport from Peripheral Tissues to the Liver Free (non-esterified) cholesterol (FC) is believed to be transferred to small HDL particles (HDL-3) by multiple mechanisms. Cholesterol in HDL-3 is esterified by lecithin-cholesterol acyl transferase (LCAT), which expands HDL particle size (HDL-2). A portion of cholesterol ester is transferred to very-low-density lipoproteins (VLDL). This transfer is mediated by cholesterol ester transfer protein (CETP). VLDL triglyceride is removed by lipolysis, which converts VLDL to low-density lipoprotein (LDL). The latter is removed by the liver through LDL receptors (LDLR). This represents one pathway of reverse cholesterol transport. A second way is through uptake of cholesterol esters from HDL-2 via scavenger receptor-B1 (SR-B1) located on liver and adrenal gland. In the liver, cholesterol ester is de-esterified and excreted in the bile (or converted to bile acids). In the adrenal gland, cholesterol is used as a precursor for synthesis of steroid hormones. Removal of cholesterol ester from HDL-2 transforms HDL back to HDL-3. Cell Metabolism 2016 23, 755-757DOI: (10.1016/j.cmet.2016.04.019) Copyright © 2016 Terms and Conditions