The Concept of CMR
Intra-abdominal Adipose Tissue: the Culprit?
- 1Key Points (1 page)
- 2Overview (1 page)
- 3Intravascular Lipid Transport in the Fasted State (4 pages)
- 4Intravascular Transport of Dietary Fat (1 page)
- 5The Dyslipidemic Profile of Intra-abdominal Obesity and the Metabolic Syndrome (7 pages)
- 6References (1 page)
- 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.