1. Schematic overview of the role of LCAT in lipoprotein metabolism
Schematic overview of the role of LCAT in lipoprotein metabolism. Triglyceride-rich apo B–containing lipoproteins are secreted from the intestine and liver. The triglycerides on plasma lipoproteins are hydrolyzed by lipoprotein lipase (LPL) and the particles are remodeled to smaller, very low density lipoproteins (VLDLs) and finally to intermediate-density lipoproteins (IDLs). VLDLs and IDLs may be removed by the liver by the low-density lipoprotein receptor (LDL-R) and low-density lipoprotein–related protein (LRP), or the cholesterol may be selectively removed from the apo B–containing lipoproteins by the scavenger receptor BI (SR-BI). IDLs are converted to low-density lipoproteins (LDLs) by the combined action of LPL and hepatic lipase (HL). LDL is taken up by cells by LDL-R–mediated endocytosis or becomes oxidized and removed from plasma by scavenger receptor A (SRA) or CD36. Nascent HDL facilitates the removal of cellular cholesterol from peripheral cells via the newly described ABC1 transporter.87 LCAT catalyzes the esterification of cholesterol to cholesterol esters (CEs), which is associated with the maturation of the nascent disk-shaped HDL to spherical particles. Cholesterol ester transfer protein (CETP) exchanges HDL-CE and triglycerides on apo B–containing lipoproteins. HDL-CE may be selectively taken up by SR-BI in the liver, and the major sites of catabolism of HDL are the liver and kidney.
Source: Lecithin Cholesterol Acyltransferase Deficiency and Fish Eye Disease, The Online Metabolic and Molecular Bases of Inherited Disease
Citation: Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson K, Mitchell G. The Online Metabolic and Molecular Bases of Inherited Disease; 2014 Available at: Accessed: October 16, 2017
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