Exogenous and endogenous fat-transport pathways are diagrammed. Dietary cholesterol is absorbed through the wall of the intestine and is packaged, along with triglyceride (glycerol ester-linked to three fatty acid chains), in chylomicrons. In the capillaries of fat and muscle tissue the triglyceride's ester bond is cleaved by the enzyme lipoprotein (LP) lipase and the fatty acids are removed. When the cholesterol-rich remnants reach the liver, they bind to specialized receptors and are taken into liver cells. Their cholesterol either is secreted into the intestine (mostly as bile acids) or is packaged with triglyceride in very-low-density lipoprotein (VLDL) particles and secreted into the circulation, inaugurating the endogenous pathway. Again the triglyceride is removed in fat or muscle, leaving cholesterol-rich intermediate-density lipoprotein (IDL). Some IDL binds to liver LDL receptors and is rapidly taken up by liver cells; the remainder stays in the circulation and is converted into LDL. Most of the LDL binds to LDL receptors on liver or other cells and is removed from the circulation. Cholesterol leaching from cells binds to high-density lipoprotein (HDL) and is esterified by the enzyme LCAT. The esters are transferred to IDL and then LDL and are eventually taken up again by cells. From Brown MS, Goldstein JS. How HDL receptors influence cholesterol and atherosclerosis. Copyright © 1984 by Scientific American, Inc. All rights reserved.