Chylomicron remnant and very-low-density lipoprotein remnant particle

Chylomicron remnant and very-low-density lipoprotein remnant particles are intermediate lipoprotein particles formed during the metabolism of chylomicrons and VLDL, respectively. Chylomicron remnants arise after triglyceride-rich chylomicrons (from intestinal absorption of dietary fat) lose much of their triglyceride core through the action of lipoprotein lipase, resulting in cholesterol-rich particles that are efficiently taken up by the liver, mainly via hepatic receptors recognizing apolipoprotein E[4][5][6]. VLDL remnants, also termed intermediate-density lipoproteins (IDL), are similarly formed after partial lipolysis of VLDL by lipoprotein lipase, before further conversion to low-density lipoprotein (LDL) or hepatic uptake[1][2][3]. Both types of remnants are enriched in cholesteryl esters and are considered more atherogenic than native VLDL or LDL, as they can penetrate the arterial wall, promote macrophage foam cell formation, and contribute to atherosclerosis[1][2][5]. Clearance from plasma is mediated via hepatic receptors, predominantly LDL receptor and LDL receptor-related proteins, requiring apolipoprotein E as a ligand for chylomicron remnant uptake[2][4]. Elevations in remnant lipoproteins are associated with increased cardiovascular disease risk and are characteristic of certain dyslipidemias (e.g., type III hyperlipidemia)[2][1]. These particles are functional lipid carriers rather than classical molecular targets (e.g., receptors or enzymes), so listing them as a "target" for drug action is atypical; instead, they are biological mediators of risk and indirect targets of therapy aimed at modifying their concentration or composition[1][2][4][5].

Other names

Chylomicron remnantVLDL remnanttriglyceride-rich lipoprotein remnantremnant lipoprotein particleintermediate-density lipoproteinIDLRLP

Enhance clearance of remnants via upregulation of hepatic remnant receptors (e.g., LDL receptor); Inhibit production or secretion of chylomicrons/VLDL (e.g., by modulating apolipoprotein or microsomal triglyceride transfer protein); Inhibit cholesteryl ester transfer protein to reduce remnant cholesterol enrichment