Abstract |
Exaggerated postprandial hypertriglyceridemia is a risk factor for cardiovascular disease. This metabolic abnormality is principally due to overproduction and/or decreased catabolism of triglyceride-rich lipoproteins (TRLs) and is a consequence of pathogenic genetic variations and other coexistent medical conditions, particularly obesity and insulin resistance. Accumulation of TRL in the postprandial state promotes the formation of small, dense low-density lipoproteins, as well as oxidative stress, inflammation, and endothelial dysfunction, all of which compound the risk of cardiovascular disease. The cardiovascular benefits of lifestyle modification ( weight loss and exercise) and conventional lipid-lowering therapies ( statins, fibrates, niacin, ezetimibe, and n-3 fatty acid supplementation) could involve their favorable effects on TRL metabolism. New agents, such as dual peroxisome-proliferator-activated receptor α/δ agonists, diacylglycerol, inhibitors of diacylglycerol acyltransferase 1 and microsomal triglyceride transfer protein, antisense oligonucleotides for apolipoprotein B-100 and apolipoprotein C-III, and incretin-based therapies, may enhance the treatment of postprandial lipemia, but their efficacy needs to be tested in clinical end point trials. Further work is required to develop a simple clinical protocol for investigating postprandial lipemia, as well as internationally agreed management guidelines for this type of dyslipidemia.
|
Authors | D C Chan, J Pang, G Romic, G F Watts |
Journal | Current atherosclerosis reports
(Curr Atheroscler Rep)
Vol. 15
Issue 3
Pg. 309
(Mar 2013)
ISSN: 1534-6242 [Electronic] United States |
PMID | 23345190
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
|
Chemical References |
|
Topics |
- Cardiovascular Diseases
(epidemiology, etiology, therapy)
- Humans
- Hypertriglyceridemia
(complications, drug therapy, metabolism)
- Hypolipidemic Agents
(therapeutic use)
- Postprandial Period
- Treatment Outcome
|