| Abstract
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No abstract available. Extract: Apolipoprotein CIII (apoCIII)
was first identified more than 40 years ago as a component of
very-low-density lipoprotein (VLDL)1 and shortly thereafter as
an inhibitor of lipoprotein lipase.2 More than a decade later,
apoCIII was found to inhibit lipoprotein remnant uptake by the
liver.3 Its relevance to human lipid metabolism was made clear
by its absence, along with apolipoprotein AI, in 2 sisters with
essentially no plasma high-density lipoprotein and very low triglyceride
levels.4 These individuals had marked increases in the fractional
removal of TG from VLDL (increased lipoprotein lipase activity)
and increased conversion of VLDL to low-density lipoprotein (LDL)
(less remnant removal). These findings spurred investigations
at a molecular level, including demonstrations of hypertriglyceridemia
in apoCIII transgenic mice6 and decreased TG levels in apoCIII
knockout mice.7 In humans, apoCIII levels are associated with
hypertriglyceridemia and increases in VLDL and inversely related
to the size of LDL particles. ApoCIII was the first lipid-associated
gene to be linked by a common polymorphism to hypertriglyceridemia.
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