The focus of this review is on the role of
apolipoprotein C-II (
apoC-II) in
lipoprotein metabolism and the potential effects on the risk of
cardiovascular disease (CVD). We searched PubMed/Scopus for articles regarding
apoC-II and its role in
lipoprotein metabolism and the risk of CVD.
Apolipoprotein C-II is a constituent of
chylomicrons,
very low-density lipoprotein,
low-density lipoprotein, and
high-density lipoprotein (HDL).
Apolipoprotein C-II contains 3 amphipathic α-helices. The
lipid-binding domain of
apoC-II is located in the N-terminal, whereas the C-terminal helix of
apoC-II is responsible for the interaction with
lipoprotein lipase (LPL). At intermediate concentrations (approximately 4 mg/dL) and in normolipidemic subjects,
apoC-II activates LPL. In contrast, both an excess and a deficiency of
apoC-II are associated with reduced LPL activity and
hypertriglyceridemia. Furthermore, excess
apoC-II has been associated with increased
triglyceride-rich particles and alterations in HDL particle distribution, factors that may increase the risk of CVD. However, there is not enough current evidence to clarify whether increased
apoC-II causes
hypertriglyceridemia or is an epiphenomenon reflecting
hypertriglyceridemia. A number of
pharmaceutical interventions, including
statins,
fibrates,
ezetimibe,
nicotinic acid, and
orlistat, have been shown to reduce the increased
apoC-II concentrations. An excess of
apoC-II is associated with increased
triglyceride-rich particles and alterations in HDL particle distribution. However, prospective trials are needed to assess if
apoC-II is a CVD marker or a risk factor in high-risk patients.