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Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles (LDL—commonly known as "bad cholesterol" when in reference to both heart disease and vascular disease in general), which is responsible for carrying fat molecules , including cholesterol, around the body to all cells within all tissues. While ...
Apolipoprotein B deficiency is an autosomal dominant disorder resulting from a missense mutation which reduces the affinity of apoB-100 for the low-density lipoprotein receptor (LDL Receptor). This causes impairments in LDL catabolism, resulting in increased levels of low-density lipoprotein in the blood.
LDL circulates and is absorbed by the liver and peripheral cells. Binding of LDL to its target tissue occurs through an interaction between the LDL receptor and apolipoprotein B-100 on the LDL particle. Absorption occurs through endocytosis, and the internalized LDL particles are hydrolyzed within lysosomes, releasing lipids, chiefly cholesterol.
On the other hand, skipping breakfast can lead to an increased risk of heart-related complications and elevated small LDL cholesterol levels, says Melissa Russell, RDN, CSR, LDN, a registered ...
Apolipoprotein B plays a particularly important role in lipoprotein transport being the primary organizing protein of many lipoproteins. [ 1 ] Apolipoprotein C-III (apoC3) plays an important role in lipid metabolism specific in regulating the metabolism of triglyceride-rich lipoproteins (TRLs).
Lipoproteins transfer lipids around the body in the extracellular fluid, making fats available to body cells for receptor-mediated endocytosis. [2] [3] Lipoproteins are complex particles composed of multiple proteins, typically 80–100 proteins per particle (organized by a single apolipoprotein B for LDL and the larger particles).
Chylomicron structure ApoA, ApoB, ApoC, ApoE (apolipoproteins); T (triacylglycerol); C (cholesterol); green (phospholipids). Chylomicrons transport lipids absorbed from the intestine to adipose, cardiac, and skeletal muscle tissue, where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty acids to be absorbed by the tissues.
It is caused by a mutation in microsomal triglyceride transfer protein resulting in deficiencies in the apolipoproteins B-48 and B-100, which are used in the synthesis and exportation of chylomicrons and VLDL respectively. It is not to be confused with familial dysbetalipoproteinemia. It is a rare autosomal recessive disorder. [4]