Chylomicrons (dietary) and VLDL (endogenous) are the main triglyceride carriers in the blood. LDL and HDL are the main cholesterol carriers.
LDL delivers cholesterol to peripheral tissues. HDL delivers cholesterol from tissues to the liver.
The ‘traditional’ dyslipidemia typically associated with intra-abdominal (visceral) obesity includes hypertriglyceridemia, the presence of small, dense LDL, and low HDL cholesterol levels. All three abnormalities are metabolically linked.
Chylomicron and VLDL remnants (not routinely measured) are also elevated in intra-abdominal obesity.
Under pro-atherogenic conditions, chylomicron remnants, VLDL remnants, and small LDL deliver cholesterol to the artery wall (pro-atherogenic). HDL removes cholesterol from the artery wall (anti-atherogenic).
Insulin resistance plays a key role in linking intra-abdominal obesity and dyslipidemia.
A newer set of metabolic risk factors—the ‘atherogenic metabolic triad’—includes hyperinsulinemia, hyperapo B, and small LDL particles. These risk factors enable additional subjects at risk of CVD to be identified.
A number of drugs are available to treat each component of the dyslipidemia of intra-abdominal obesity. But a key therapeutic objective remains the reduction of intra-abdominal fat, the primary cause of dyslipidemia.
Evaluation of the association between the first observation and the longitudinal change in C-reactive protein, and all-cause mortality. Heart 2008;94:457-62