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    An ABC of apolipoprotein C-III: a clinically useful new cardiovascular risk factor?

    Access Status
    Fulltext not available
    Authors
    Chan, D.
    Chen, Meifania
    Ooi, E.
    Watts, G.
    Date
    2008
    Type
    Journal Article
    
    Metadata
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    Citation
    Chan, Dick and Chen, Meifania and Ooi, Esther and Watts, Gerald. 2008. An ABC of apolipoprotein C-III: a clinically useful new cardiovascular risk factor?. International Journal of Clinical Practice. 62 (5): pp. 799-809.
    Source Title
    International Journal of Clinical Practice
    DOI
    10.1111/j.1742-1241.2007.01678.x
    ISSN
    17421241
    Faculty
    Curtin Business School
    School
    Centre for Extended Enterprises and Business Intelligence
    Remarks

    Copyright © 2008 John Wiley & Sons, Inc. All Rights Reserved.

    The link to the published version is available at: http://www3.interscience.wiley.com/journal/119418283/abstract

    URI
    http://hdl.handle.net/20.500.11937/22580
    Collection
    • Curtin Research Publications
    Abstract

    Background: Hypertriglyceridaemia, commonly found in subjects with obesity and type 2 diabetes mellitus, is associated with increased risk of coronary heart disease (CHD). Apolipoprotein C-III (apoC-III) plays an important role in regulating the metabolism of triglyceride-rich lipoproteins (TRLs) and may provide a new approach to assessing hypertriglyceridaemia. Aims: We review the role of apoC-III in regulating TRL metabolism and address the potential importance of apoC-III in clinical practice. Discussion: Hypertriglyceridaemia is chiefly a consequence of alterations in the kinetics of TRLs, including overproduction and delayed clearance of very-low density lipoprotein (VLDL). ApoC-III is an inhibitor of lipoprotein lipase and of TRLs remnant uptake by hepatic lipoprotein receptors. Elevated apoC-III, usually resulting from hepatic overproduction of VLDL apoC-III, may cause accumulation of plasma TRLs leading to hypertriglyceridaemia. The results from recent observational studies demonstrate that apoC-III is a strong predictor of risk for CHD, but this chiefly relates to apoC-III in apoB-containing lipoproteins. Lifestyle and pharmacological intervention can correct hypertriglyceridaemia by a mechanism of action that regulates apoC-III transport. Conclusions: Targeting apoC-III metabolism may therefore be an important, new therapeutic approach to managing dyslipidaemia and CHD risk in obesity, insulin resistance and type 2 diabetes mellitus. However, further work is required to establish the practical aspects of measuring apoC-III in routine laboratory service and the precise therapeutic targets for serum total apoC-III and/or apoC-III in apoB-containing lipoproteins. While showing much promise as a potentially useful cardiovascular risk factor, apoC-III is not yet ready for prime time use in clinical practice.

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