The Concept of CMR

Intra-abdominal Adipose Tissue: the Culprit?

Atherogenic Dyslipidemia

Key Points

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  • 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.