Scavenger receptor. Like chylomicron remnants, the triglyceride-poor VLDL remnants may reenter the liver. Chylomicron remnants can also remain sequestered in the space of Disse by binding of apoE to heparan sulfate proteoglycans and/or binding of apoB-48 to hepatic lipase. Chylomicron remnant. It has ApO B48 and ApO E, but the ApO C2 is returned to HDL. Present on nearly all cells and account for 70-80% of LDL catabolism. Remnant receptor (Apo-E) Found in the liver only. What happens to remnant chylomicrons in the liver? Chylomicron remnant clearance is mediated by the action of lipoprotein Summary Chylomicron metabolism starts with the absorption of dietary lipids by intestinal epithelial cells. What is the point of ApO E? Next, MTP lipidates the chylomicron structural protein, Apo B-48. For competition studies, a lO-fold excess of un­ labelJed chylomicron remnants or LOL receptor antibody (3,7JJg/mL protein) was included in the incubation buffer containing gold--chylomicron remnant conjugates. APOB48 and APOE are important for the identification of chylomicron remnants in the liver due to endocytosis and degradation. Introduction Chylomicron remnants are potentially atherogenic lipoproteins [1]4]. Chylomicron Remnant: When the triglyceride reserve consumes (distributed), it converts APOC2 back to HDL (which APOE retains), leaving chylomicrons remnants of only 20-50 nm. hypercholesterolaemia (FH), remnant receptor & triglycerides. Delivers cholesterol to liver and it is not regulated. The lipidated Apo B-48 is now termed a chylomicron, and it is composed primarily of dietary triglycerides. Previously, it was shown that canine HDL c was a competitive inhibitor of chylomicron remnants for uptake by the perfused rat liver , and in addition to their ability to bind with high affinity to the LDL receptor (1, 49), HDL c have now been demonstrated to bind to … Remnants derived from VLDL are found mainly in the IDL (d = 1.006–1.019 g/mL) range after ultracentrifugation, although some are also present in the VLDL density range (d < 1.006 g/mL). The major determinant of LDL concentration in plasma is the number/activity of LDL receptors. Interaction of chylomicron remnants with the LDL receptor-related protein, or another endocytic receptor with similar properties, occurs slowly, requiring modification of surface-bound chylomicron remnants, and serves as a backup mechanism that is utilized primarily when LDL receptors are deficient or down-regulated. APOB48 and APOE are important to identify the chylomicron remnant in the liver for endocytosis and breakdown. Uptake of oxidized or chemically modified LDL-Particles by Monocytes in circulation or Macrophages in tissues (these are not recognised by LDL receptor). The chylomicron remnant is picked up by hepatocytes through the apoE receptor; thus, dietary cholesterol, as well as any remaining triglyceride, is released in the hepatocyte. gold--chylomicron remnant conjugates. Once triglyceride stores are distributed, the chylomicron returns APOC2 to the HDL (but keeps APOE), and, thus, becomes a chylomicron remnant, now only 30–50 nm. Recognizes Chylomicron Remnants and Apo-E Rich HDL receptors. VLDL (Very Low-Density Lipoprotein) Unlike chylomicrons, the VLDL remnants may be further metabolized to become LDL. Defective chylomicron-remnant removal but normal LDL clearance in the heterozygote WHHL corresponded to elevated concentrations of plasma triacylglycerol and normal concentrations of plasma cholesterol. Let’s compare Chylomicrons with other terms. 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