Plasma kinetics of apoC-III and apoE in normolipidemic and hypertriglyceridemic subjects.
Open accessAbstract
Apolipoprotein (apo) C-III and apoE play a central role in controlling the plasma metabolism of triglyceride-rich lipoproteins (TRL). We have investigated the plasma kinetics of total, very low density lipoprotein (VLDL) and high density lipoprotein (HDL) apoC-III and apoE in normolipidemic (NL) (n = 5), hypertriglyceridemic (HTG, n = 5), and Type III hyperlipoproteinemic (n = 2) individuals. Apolipoprotein kinetics were investigated using a primed constant (12 h) infusion of deuterium-labeled leucine. HTG and Type III patients had reduced rates of VLDL apoB-100 catabolism and no evidence of VLDL apoB-100 overproduction. Elevated (3- to 12-fold) total plasma and VLDL apoC-III levels in HTG and Type III patients, although associated with reduced apoC-III catabolism (i.e., increased residence times (RTs)), were mainly due to increased apoC-III production (plasma apoC-III transport rates (TRs, mean +/- SEM): (NL) 2.05 +/- 0.22 (HTG) 4.90 +/- 0.81 (P < 0.01), and (Type III) 8.78 mg. kg(-)(1). d(-)(1); VLDL apoC-III TRs: (NL) 1.35 +/- 0. 23 (HTG) 5.35 +/- 0.85 (P < 0.01), and (Type III) 7.40 mg. kg(-)(1). d(-)(1)). Elevated total plasma and VLDL apoE levels in HTG (2- and 6-fold, respectively) and in Type III (9- and 43-fold) patients were associated with increased VLDL apoE RTs (0.21 +/- 0.02, 0.46 +/- 0. 05 (P < 0.01), and 1.21 days, NL vs. HTG vs. Type III, respectively), as well as significantly increased apoE TRs (plasma: (NL) 2.94 +/- 0.78 (HTG) 5.80 +/- 0.59 (P < 0.01) and (Type III) 11.80 mg. kg(-)(1). d(-)(1); VLDL: (NL) 1.59 +/- 0.18 (HTG) 4.52 +/- 0.61 (P < 0.01) and (Type III) 11.95 mg. kg(-)(1). d(-)(1)). These results demonstrate that hypertriglyceridemic patients, having reduced VLDL apoB-100 catabolism (including patients with type III hyperlipoproteinemia) are characterized by overproduction of plasma and VLDL apoC-III and apoE.
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The increase in triglyceride production may be due to excess free fatty acids returning to the liver, particularly in visceral obesity and insulin resistance, and increased de novo triglyceride production due to hyperinsulinemia.
“The increase in triglyceride production may be due to excess free fatty acids returning to the liver, particularly in the setting of visceral obesity and insulin resistance, and increased de novo triglyceride production due to hyperinsulinemia (24,62,63).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [62]
Defective clearance of triglyceride-rich VLDL by LpL can contribute to moderate hypertriglyceridemia, and many patients have overproduction of VLDL triglyceride in the liver with increased secretion.
“Defective clearance of triglyceride-rich VLDL by LpL can contribute to this condition, and many patients have overproduction of VLDL triglyceride in the liver with an increased secretion (24,62,63).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [62]
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 [24]
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References 62 · Cited by 113
- Authors
- Batal, R., Tremblay, M., Barrett, P. H. R., Jacques, H., Fredenrich, A., Mamer, O., Davignon, J., & Cohn, J. S.
- Affiliations
- The University of Western Australia (AU)
- McGill University (CA)
- Corresponding author
- Cohn, Jeffrey S.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2000-05
- Volume
- 41
- Issue
- 5
- Pages
- 706-718
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W1900613292
- Cited by
- 113
- References
- 62
- Citations by year
- 2025: 1 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 9 · 2014: 5 · 2013: 2 · 2012: 3
- FWCI
- 4.94
- 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 › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- apolipoprotein C-III, apolipoprotein E, plasma kinetics, hypertriglyceridemia, type III hyperlipoproteinemia, triglyceride-rich lipoproteins, lipoprotein metabolism
- MeSH terms
- Adult, Apolipoproteins B, Apolipoproteins C, Apolipoproteins E, Female, Humans, Kinetics, Lipoproteins, HDL, Lipoproteins, VLDL, Male, Middle Aged, Reference Values, Triglycerides, Hypertriglyceridemia, Case-Control Studies, Apolipoprotein B-100, Apolipoprotein C-III
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