Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Conference paper

Publication Date

05/2002

Volume

3

Pages

41 - 46

Keywords

Clinical Trials as Topic, Coronary Disease, Drug Therapy, Combination, Gemfibrozil, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipidemias, Hypolipidemic Agents, Lipid Metabolism, Postprandial Period, Simvastatin