Kylomikronremnants

Kylomikronremnants, more commonly known as chylomicron remnants, are the lipoprotein particles left after chylomicrons transport dietary triglycerides to body tissues. Chylomicrons are formed in enterocytes, contain apoB-48 as their main structural apolipoprotein, and acquire apoC-II and apoE from high-density lipoproteins in the bloodstream.

After entering circulation, lipoprotein lipase on capillary endothelium hydrolyzes the triglycerides within chylomicrons, releasing fatty acids for use by muscle and adipose tissue. This lipolysis converts chylomicrons into smaller, cholesterol-rich remnants that are depleted of triglycerides and enriched in cholesterol esters and apoE. Chylomicron remnants are rapidly cleared from the bloodstream by the liver, primarily through receptor-mediated uptake involving apoE and members of the LDL receptor family, such as the LDL receptor and LRP1.

Clinically, efficient clearance of chylomicron remnants helps terminate postprandial lipemia and limits remnant-associated cholesterol delivery to the arterial wall. Impaired remnant clearance can lead to elevated postprandial triglyceride-rich lipoproteins and contribute to atherogenic risk. A notable genetic disorder affecting remnant handling is familial dysbetalipoproteinemia (type III), caused by apolipoprotein E2/E2, which reduces hepatic uptake of remnants and leads to accumulation of chylomicron and VLDL remnants. In general, remnants and remnant cholesterol are recognized as factors in cardiovascular risk and are a focus of lipid research and clinical assessment.