Cited by 85Lipid metabolism and disordersLipoproteins and Cardiovascular HealthDiabetes, Cardiovascular Risks, and Lipoproteins

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

Open access
Chan, D. C., Chen, M. M., Ooi, E. M. M., Watts, G. F.·2008·International Journal of Clinical Practice

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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Crossref · 10.1111/j.1742-1241.2007.01678.x

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  • ApoC-I, apoC-II, and apoC-III are involved in the uptake or degradation of triglycerides, chylomicron remnants, and cholesterol-rich lipoproteins by regulation of lipoprotein lipase.

    “ApoC-I, apoC-II, and apoC-III are involved in the uptake or degradation of triglycerides, chylomicron remnants, and cholesterol-rich lipoproteins by regulation of lipoprotein lipase (4-7) .”

    From Automated multiplex LC-MS/MS assay for quantifying serum apolipoproteins A-I, B, C-I, C-II, C-III, and E with qualitative apolipoprotein E phenotyping (2016) · cites this paper as [4]

    The ApoC-III: structure and function section says apoC-III inhibits lipoprotein lipase (LPL), while apoC-II is an LPL cofactor; the Review Criteria section links both to VLDL triglyceride breakdown. The paper does not establish an LPL-regulating role for apoC-I. It also describes clearance of cholesterol-rich chylomicron remnants by hepatic receptors, not by LPL. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • ApoC-III serves as an independent risk marker for CVD due to its central role in lipid metabolism.

    “ApoC-III serves as an independent risk marker for CVD due to its central role in lipid metabolism [164, 165].”

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Research works printed but not linked: 3

  1. [31]31. Sundaram M, Links P, Khalil MB, Zhong S, Yao Z. New insights into the roles of apolipoprotein C-III in stimulating the produc- tion of hepatic VLDL. Arterioscler Thromb Vasc Biol 2007; 27: e62.
  2. [34]34. Ito Y, Azrolan N, O'Connell A, Walsh A, Breslow JL. Hypertrigly- ceridemia as a result of human apo CIII gene expression in trans- genic mice. Science 1990; 249: 790-3.
  3. [48]48. Peacock RE, Temple A, Gudnason V, Rosseneu M, Humphries SE. Variation at the lipoprotein lipase and apolipoprotein AI-C-III gene loci are associated with fasting lipid and lipoprotein traits in a population sample from Iceland: interaction between genotype, gender, and smoking status. Genet Epidemiol 1997; 14: 265-82.

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Authors
Chan, D. C., Chen, M. M., Ooi, E. M. M., & Watts, G. F.
Affiliations
The University of Western Australia (AU)
Corresponding author
Watts, G. F.
Venue
International Journal of Clinical Practice
Published
2008-01-14
Volume
62
Issue
5
Pages
799-809
ISSN
1368-5031 (ISSN-L)
OpenAlex
W1924220480
Cited by
85
References
93
Citations by year
2026: 3 · 2025: 3 · 2024: 8 · 2023: 10 · 2022: 5 · 2021: 1 · 2020: 7 · 2019: 4 · 2017: 1 · 2016: 3 · 2015: 5 · 2014: 3 · 2013: 9 · 2012: 5
FWCI
0.91
Type
journal article
Language
en
Open access
Locations
  • International Journal of Clinical Practice (publishedVersion)
  • PubMed (publishedVersion)
  • UWA Profiles and Research Repository (UWA) (submittedVersion)
  • eSpace (Curtin University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
apolipoprotein C-III, hypertriglyceridemia, triglyceride-rich lipoproteins, VLDL, lipoprotein lipase inhibition, coronary heart disease risk, cardiovascular risk factors, type 2 diabetes, obesity, insulin resistance, dyslipidemia, apoB-containing lipoproteins
MeSH terms
Cardiovascular Diseases, Humans, Risk Factors, Triglycerides, Hypertriglyceridemia, Biomarkers, Metabolic Syndrome, Apolipoprotein C-III

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