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dc.contributor.authorKei, A. A.en
dc.contributor.authorFilippatos, T. D.en
dc.contributor.authorTsimihodimos, V.en
dc.contributor.authorElisaf, M. S.en
dc.date.accessioned2015-11-24T19:39:13Z-
dc.date.available2015-11-24T19:39:13Z-
dc.identifier.issn1532-8600-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24224-
dc.rightsDefault Licence-
dc.titleA review of the role of apolipoprotein C-II in lipoprotein metabolism and cardiovascular diseaseen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.metabol.2011.12.002-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/22304839-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0026049511004112/1-s2.0-S0026049511004112-main.pdf?_tid=ad272f14bf8a0a8e62987c22f6670853&acdnat=1333532152_36db3edf4b5249f540090962fb72f44b-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2012-
heal.abstractThe focus of this review is on the role of apolipoprotein C-II (apoC-II) in lipoprotein metabolism and the potential effects on the risk of cardiovascular disease (CVD). We searched PubMed/Scopus for articles regarding apoC-II and its role in lipoprotein metabolism and the risk of CVD. Apolipoprotein C-II is a constituent of chylomicrons, very low-density lipoprotein, low-density lipoprotein, and high-density lipoprotein (HDL). Apolipoprotein C-II contains 3 amphipathic alpha-helices. The lipid-binding domain of apoC-II is located in the N-terminal, whereas the C-terminal helix of apoC-II is responsible for the interaction with lipoprotein lipase (LPL). At intermediate concentrations (approximately 4 mg/dL) and in normolipidemic subjects, apoC-II activates LPL. In contrast, both an excess and a deficiency of apoC-II are associated with reduced LPL activity and hypertriglyceridemia. Furthermore, excess apoC-II has been associated with increased triglyceride-rich particles and alterations in HDL particle distribution, factors that may increase the risk of CVD. However, there is not enough current evidence to clarify whether increased apoC-II causes hypertriglyceridemia or is an epiphenomenon reflecting hypertriglyceridemia. A number of pharmaceutical interventions, including statins, fibrates, ezetimibe, nicotinic acid, and orlistat, have been shown to reduce the increased apoC-II concentrations. An excess of apoC-II is associated with increased triglyceride-rich particles and alterations in HDL particle distribution. However, prospective trials are needed to assess if apoC-II is a CVD marker or a risk factor in high-risk patients.en
heal.journalNameMetabolismen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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