Abstract |
Exaggerated postprandial hyperlipidemia has been associated with cardiovascular disease. The mechanisms underlying this association are likely to depend on a multitude of effects. Potentially atherogenic remnants of triglyceride-rich lipoproteins (TRL) accumulate in the postprandial state. In addition, TRL may promote the formation of small dense LDL. There are some indications that the postprandial period is a hypercoagulable state and endothelial function seems to be hampered after acute fat intake. Conventional lipid lowering drugs such as statins and fibrates have the potency of reducing postprandial hyperlipidemia, but the fibrates seem to be more effective in this respect. There is a complete lack of prospective studies linking inefficient postprandial lipid metabolism with clinical endpoints and there is also a need to include investigations of postprandial lipid metabolism in the evaluation of novel drugs affecting lipid metabolism and insulin resistance.
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Authors | Fredrik Karpe |
Journal | Atherosclerosis. Supplements
(Atheroscler Suppl)
Vol. 3
Issue 1
Pg. 41-6
(May 2002)
ISSN: 1567-5688 [Print] Netherlands |
PMID | 12044585
(Publication Type: Journal Article, Review)
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Chemical References |
- Hydroxymethylglutaryl-CoA Reductase Inhibitors
- Hypolipidemic Agents
- Simvastatin
- Gemfibrozil
|
Topics |
- Clinical Trials as Topic
- Coronary Disease
(etiology)
- Drug Therapy, Combination
- Gemfibrozil
(therapeutic use)
- Humans
- Hydroxymethylglutaryl-CoA Reductase Inhibitors
(therapeutic use)
- Hyperlipidemias
(complications, drug therapy)
- Hypolipidemic Agents
(therapeutic use)
- Lipid Metabolism
- Postprandial Period
- Simvastatin
(therapeutic use)
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