Inside a medical journal
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In healthy people, plasma cholesterol exists in a variety of forms including VLDL, IDL and LDL. Liver cells secrete VLDL, which has three surface apolipoproteins: ApoE, B-100 and ApoC. VLDL undergoes lipolysis in capillaries of adipose tissue or muscle, which extracts triglycerides from the molecule. This converts it into IDL, which has also lost the membrane protein ApoC. Around 50% of IDL is taken up by liver cells via receptors for B-100 or ApoE; whatever remains undergoes further metabolic processes and is converted into LDL, which only has the B-100 membrane protein. LDL is then taken up by liver cells to undergo cholesterol metabolism and be recycled as VLDL.
In familial hypercholesterolemia, a mutation in the receptor for apolipoprotein B-100 interferes with this process. LDL cannot be removed from the plasma, and less IDL is taken up, resulting in increased production of LDL. Homozygotes with this mutation have 5-6 times higher levels of LDL than a healthy person, and are susceptible to developing skin xanthomas and atherosclerosis.
Source: Kumar, V. et al., 2009. Robbins & Cotran Pathologic Basis of Disease, Elsevier Health Sciences.