The role of scavenger receptor BI in hepatitis - eTheses Repository ...

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intricate network of interactions between the lipoproteins, apoproteins,
enzymes and receptors, which naturally lends it self to adaptability. It would
be inappropriate to cover this in great detail here, therefore the following
paragraphs summarise the journey of dietary lipids entering and exiting the
lipoprotein pathway.
Upon entering the intestine, dietary lipids are emulsified, taken up by
enterocytes and used to assemble CM, each containing a single ApoB-48
molecule. CM enter circulation via the lymphatic system and quickly acquire
exchangeable ApoC-II molecules. ApoC-II facilitates the action of lipoprotein
lipase (LPL), an enzyme that releases fatty acids from TG. As the TG is
depleted from CM ApoC-II is replaced by ApoE, which facilitates the uptake of
CM by the liver, delivering the remaining TGs and cholesterol to the hepatic
lipoprotein assembly pathway.
As the site of VLDL assembly the liver is central to controlling plasma
lipoprotein concentrations. Microsomal triglyceride transfer protein (MTP),
loads ApoB-100 molecules with lipid to form nascent VLDL particles. As these
move through the secretory pathway they become increasingly lipidated a
process facilitated by the addition of ApoE (122). ApoB-100 is constitutively
produced by hepatocytes however poorly lipidated forms are degraded before
secretion. Once in the circulation the action of lipases such as LPL depletes
VLDL of tri-glycerides, leading to a gradual enrichment of cholesterol and loss
of the exchangeable apoproteins. This culminates in LDL, a smaller, more
dense particle. LDL is the major carrier of cholesterol throughout the body,