Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects
Open accessAbstract
ApoC-I has several different lipid-regulating functions including, inhibition of receptor-mediated uptake of plasma triglyceride-rich lipoproteins, inhibition of cholesteryl ester transfer activity, and mediation of tissue fatty acid uptake. Since little is known about the rate of production and catabolism of plasma apoC-I in humans, the present study was undertaken to determine the plasma kinetics of VLDL and HDL apoC-I using a primed constant (12 h) intravenous infusion of deuterium-labeled leucine. Data were obtained for 14 subjects: normolipidemics (NL, n = 4), hypertriglyceridemics (HTG, n = 4) and combined hyperlipidemics (CHL, n = 6). Plasma VLDL triglyceride (TG) levels were 0.59 +/- 0.03, 4.32 +/- 0.77 (P < 0.01 vs. NL), and 2.20 +/- 0.39 mmol/l (P < 0.01 vs. NL), and plasma LDL cholesterol (LDL-C) levels were 2.34 +/- 0.22, 2.48 +/- 0.26, and 5.35 +/- 0.48 mmol/l (P < 0.01 vs. NL), respectively. HTG and CHL had significantly (P < 0.05) increased levels of total plasma apoC-I (12.5 +/- 1.2 and 12.4 +/- 1.3 mg/dl, respectively) versus NL (7.9 +/- 0.6 mg/dl), due to significantly (P < 0.01) elevated levels of VLDL apoC-I (5.8 +/- 0.8 and 4.5 +/- 0.8 vs. 0.3 +/- 0.1 mg/dl). HTG and CHL also had increased rates of VLDL apoC-I transport (i.e., production) versus NL: 2.29 +/- 0.34 and 3.04 +/- 0.53 versus 0.24 +/- 0.11 mg/kg.day (P < 0.01), with no significant change in VLDL apoC-I residence times (RT): 1.16 +/- 0.12 versus 0.69 +/- 0.06 versus 0.74 +/- 0.17. Although HDL apoC-I concentrations were not significantly lower in HTG and CHL versus NL, HDL apoC-I rates of transport were inversely related to plasma and VLDL-TG levels (r = -0.63 and -0.62, respectively, P < 0.05). Our results demonstrate that increased levels of plasma and VLDL apoC-I in hypertriglyceridemic subjects (with or without elevated LDL-C levels) are associated with increased levels of plasma VLDL apoC-I production.
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ApoC-I, apoC-III, and apoE recovered in the d>1.21 g/ml fraction were included in HDL fractions, which were corrected so that total apolipoprotein recovery after ultracentrifugation was 100%.
“As explained before (24-26), apoC-I, apoC-III, and apoE recovered in the d Ͼ 1.21 g/ml fraction (1.9 Ϯ 0.4%, 0.5 Ϯ 0.1%, and 14.6 Ϯ 0.9% of total, respectively) were included in HDL fractions, which were in turn corrected so that total apolipoprotein recovery after ultracentrifugation was 100%.”
From Plasma turnover of HDL apoC-I, apoC-III, and apoE in humans (2003) · cites this paper as [26]
The Methods section says apoC-I in the bottom fractions was counted in the HDL apoC-I pool and that lipoprotein apoC-I levels were corrected to 100% recovery. The Results section places less than 3% of apoC-I in the d > 1.21 g/ml fraction. This paper does not establish the corresponding treatment or quoted percentages for apoC-III and apoE, nor the exact 1.9 ± 0.4% figure for apoC-I. (LLM, conf=0.87)
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Research works printed but not linked: 3
- [1]1. Jong, M.C. ∙ Hofker, M.H. ∙ Havekes, L.M. Role of apoCs in lipoprotein metabolism. Functional differences between apoC1, apoC2, and apoC3 Arterioscler. Thromb. Vasc. Biol. 1999; 19:472-484 Crossref PubMed Google Scholar
- [2]2. Shachter, N.S. Apolipoproteins C–I and C–III as important modulators of lipoprotein metabolism Curr. Opin. Lipidol. 2001; 12:297-304 Crossref Scopus (259) PubMed Google Scholar
- [3]3. Jackson, R.L. ∙ Sparrow, J.T. ∙ Baker, H.N. ... The primary structure of apolipoprotein-serine J. Biol. Chem. 1974; 249:5308-5313
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Plasma turnover of HDL apoC-I, apoC-III, and apoE in humans
Cohn, J. S., Batal, R., Tremblay, M., Jacques, H., Veilleux, L., Rodriguez, C., Mamer, O., & Davignon, J. (2003) · Journal of Lipid Research · doi:10.1194/jlr.m300209-jlr200 · Cited by 35 · see citing works
Self-citation
- Authors
- Cohn, J. S., Tremblay, M., Batal, R., Jacques, H., Veilleux, L., Rodriguez, C., Bernier, L., Mamer, O., & Davignon, J.
- Affiliations
- Montreal Clinical Research Institute (CA)
- McGill University (CA)
- Corresponding author
- Cohn, Jeffrey S.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2002-10
- Volume
- 43
- Issue
- 10
- Pages
- 1680-1687
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2170384815
- Cited by
- 41
- References
- 0
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 3
- FWCI
- 1.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Lipid Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- apolipoprotein C-I, VLDL, HDL cholesterol, plasma kinetics, hypertriglyceridemia, mixed dyslipidemia, triglyceride-rich lipoproteins, cholesteryl ester transfer
- MeSH terms
- Adult, Apolipoproteins C, Data Interpretation, Statistical, Deuterium, Electrophoresis, Polyacrylamide Gel, Female, Humans, Kinetics, Lipoproteins, HDL, Lipoproteins, VLDL, Male, Software, Hypertriglyceridemia
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