Cited by 70Lipid metabolism and disordersLipoproteins and Cardiovascular HealthCholesterol and Lipid Metabolism

Apolipoproteins C-III and A-V as predictors of very-low-density lipoprotein triglyceride and apolipoprotein B-100 kinetics.

Chan, Dick C., Watts, Gerald F., Nguyen, Minh N., Barrett, P. Hugh R.·2006·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

OBJECTIVE: We investigated the associations between plasma very-low-density lipoprotein (VLDL)-apolipoprotein (apo)C-III and apoA-V concentrations and the kinetics of VLDL-apoB-100 and VLDL triglycerides in 15 men. We also explored the relationship between these parameters of VLDL metabolism and VLDL-apoC-III kinetics. METHODS AND RESULTS: ApoC-III, apoB, and triglyceride kinetics in VLDL were determined using stable isotopes and multicompartmental modeling to estimate production rate (PR) and fractional catabolic rate (FCR). Plasma VLDL-apoC-III concentration was significantly and inversely associated with the FCRs of VLDL triglycerides (r=-0.610) and VLDL-apoB (r=-0.791), and positively correlated with the PR of VLDL-apoC-III (r=0.842). However, apoA-V concentration was not significantly associated with any of the kinetic variables. There was a significant association (P<0.01) between the PRs of VLDL triglycerides and VLDL-apoB (r=0.641), and between the FCRs of VLDL triglycerides and VLDL-apoB (r=0.737). In multiple regression analysis, plasma VLDL-apoC-III concentration was a significant predictor of VLDL triglyceride FCR (beta-coefficient=-0.575) and VLDL-apoB FCR (beta-coefficient=-0.839). CONCLUSIONS: Our findings suggest that increased VLDL-apoC-III concentrations resulting from an overproduction of VLDL-apoC-III are strongly associated with the delayed catabolism of triglycerides and apoB in VLDL. We also demonstrated that the kinetics of VLDL triglycerides and apoB are closely coupled. Our data do not support a role for plasma apoA-V in regulating VLDL kinetics.

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Crossref · 10.1161/01.atv.0000203519.25116.54

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  • Clearance of VLDL from the circulation is reduced in many patients with hypertriglyceridemia, in part due to saturation of triglyceride clearance.

    “Clearance of VLDL from the circulation is reduced in many patients with hypertriglyceridemia (64, 65, 73), in part due to saturation of triglyceride clearance (74).”

    From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [73]

    The Discussion (page unavailable) reports that higher VLDL-apoC-III predicted delayed catabolism of VLDL triglycerides and apoB in men with mild dyslipidemia. It does not establish reduced VLDL clearance in many patients with hypertriglyceridemia; the authors say they did not study severe hypertriglyceridemia. The separate saturation explanation is attached to citation 74, not this source. (LLM, conf=0.85)

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Research works printed but not linked: 5

  1. Chan DC, Watts GF, Redgrave TG, Mori TA, Barrett PHR. Apoli- poprotein B100 kinetics in visceral obesity: associations with plasma apolipoprotein CIII concentrations. Metabolism. 2002;51:1041-1046.
  2. Olofsson SO. ApoA-V: The regulation of a regulator of plasma triglyc- erides. Arterioscler Thromb Vasc Biol. 2005;25:1097-1099.
  3. Dwyer K, Barrett PHR, Chan D, Foo JI, Watts GF, Croft KD. Oxazo- linone derivatives of amino acids and gas chromatography-mass spec- trometry: femtogram sensitivity applied to stable isotope kinetic studies of lipoproteins. J Lipid Res. 2002;43:344 -349.
  4. Adiels M, Boren J, Caslake MJ, Stewart P, Soro A, Westerbacka J, Wennberg B, Olofsson SO, Packard C, Taskinen MR. Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dys- lipidemia. Arterioscler Thromb Vasc Biol. 2005;25:1697-1703.
  5. Ito Y, Azrolan N, O'Connell A, Walsh A, Breslow JL. Hypertriglyceri- demia as a result of human apo CIII gene expression in transgenic mice. Science. 1990;249:790 -793.

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Authors
Chan, D. C., Watts, G. F., Nguyen, M. N., & Barrett, P. H. R.
Affiliations
The University of Western Australia (AU)
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2006-03
Volume
26
Issue
3
Pages
590-596
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W2027083746
Cited by
70
References
36
Citations by year
2024: 1 · 2023: 1 · 2021: 1 · 2020: 3 · 2019: 2 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 3 · 2013: 6 · 2012: 3
FWCI
6.56
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
  • UWA Profiles and Research Repository (UWA) (submittedVersion)
Funders
  • Pfizer
  • Royal Perth Hospital Medical Research Foundation
  • Raine Medical Research Foundation
  • Medical Research Council
  • National Health and Medical Research Council
  • National Institute of Biomedical Imaging and Bioengineering (P41EB001975)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Keywords
apolipoprotein C-III, apolipoprotein A-V, VLDL, VLDL triglycerides, apolipoprotein B-100, lipoprotein kinetics, fractional catabolic rate, production rate, triglyceride catabolism, stable isotope tracers
MeSH terms
Apolipoprotein A-V, Aged, Apolipoproteins, Apolipoproteins A, Apolipoproteins B, Apolipoproteins C, Homeostasis, Humans, Leucine, Male, Middle Aged, Predictive Value of Tests, Regression Analysis, Triglycerides, Hypertriglyceridemia, Cholesterol, VLDL, Apolipoprotein B-100, Apolipoprotein C-III

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