The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins CIII and AI: evidence that apolipoprotein CIII inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo
Open accessAbstract
Previous data suggest that apolipoprotein (apo) CIII may inhibit both triglyceride hydrolysis by lipoprotein lipase (LPL) and apo E-mediated uptake of triglyceride-rich lipoproteins by the liver. We studied apo B metabolism in very low density (VLDL), intermediate density (IDL), and low density lipoproteins (LDL) in two sisters with apo CIII-apo AI deficiency. The subjects had reduced levels of VLDL triglyceride, normal LDL cholesterol, and near absence of high density lipoprotein (HDL) cholesterol. Compartmental analysis of the kinetics of apo B metabolism after injection of 125I-VLDL and 131I-LDL revealed fractional catabolic rates (FCR) for VLDL apo B that were six to seven times faster than normal. Simultaneous injection of [3H]glycerol demonstrated rapid catabolism of VLDL triglyceride. VLDL apo B was rapidly and efficiently converted to IDL and LDL. The FCR for LDL apo B was normal. In vitro experiments indicated that, although sera from the apo CIII-apo-AI deficient patients were able to normally activate purified LPL, increasing volumes of these sera did not result in the progressive inhibition of LPL activity demonstrable with normal sera. Addition of purified apo CIII to the deficient sera resulted in 20-50% reductions in maximal LPL activity compared with levels of activity attained with the same volumes of the native, deficient sera. These in vitro studies, together with the in vivo results, indicate that in normal subjects apo CIII can inhibit the catabolism of triglyceride-rich lipoproteins by lipoprotein lipase.
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“Loss-of-function variants of APOC3 that result in reduced synthesis of the protein are associated with absent or low circulating apoCIII levels, increased efficiency of TG removal from TRL, and lower plasma TG levels,59,60”
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“Individuals with LOF APOC3 variants have low plasma TG levels59,60,187 and markedly increased in vivo fractional turnover of VLDL–TG with efficient conversion of VLDL apoB to LDL, indicating increased lipolysis.59,187”
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“Apo CIII inhibits the hydrolyzing effect of lipoprotein lipase for TG-rich particles and the hepatic absorption mediated by ApoE [2,3], and also is detrimental to the elimination of ApoB lipoproteins from plasma by interrupting their capacity to bind to hepatic lipoprotein receptors [4].”
BackgroundLe, N., & Brown, W. V. (2007) · Humana Press eBooks · doi:10.1007/978-1-59259-878-6_28
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Le, N., & Brown, W. V. (2000) · doi:10.1007/978-1-4757-9310-9_5
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Ginsberg, H. N., & Goldberg, I. J. (2001) · Comprehensive physiology · doi:10.1002/j.2040-4603.2001.tb01468.x
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“In addition to its established role in lipid metabolism [14–17], elevated apoCIII levels in normolipidemic individuals with T1D have been associated with increased risk of cardiovascular disease [18].”
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Metadata
- Authors
- Ginsberg, H. N., Le, N. A., Goldberg, I. J., Gibson, J. C., Rubinstein, A., Wang-Iverson, P., Norum, R., & Brown, W. V.
- Affiliations
- Columbia University Irving Medical Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- Henry Ford Hospital (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1986-11-01
- Volume
- 78
- Issue
- 5
- Pages
- 1287-1295
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC423815
- OpenAlex
- W2057271976
- Cited by
- 424
- References
- 38
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 7 · 2022: 11 · 2021: 15 · 2020: 23 · 2019: 9 · 2018: 15 · 2017: 18 · 2016: 12 · 2015: 18 · 2014: 11 · 2013: 14 · 2012: 8
- FWCI
- 4.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-23077, HL-00949)
- National Center for Research Resources (RR 71)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Keywords
- apolipoprotein C-III, apolipoprotein A-I deficiency, lipoprotein lipase inhibition, triglyceride-rich lipoproteins, VLDL, IDL, low-density lipoprotein, fractional catabolic rate, lipoprotein catabolism, lipoprotein lipase activation
- MeSH terms
- Adult, Apolipoproteins A, Apolipoproteins B, Apolipoproteins C, Cholesterol, Humans, Hypolipoproteinemias, Kinetics, Lipoprotein Lipase, Lipoproteins, LDL, Lipoproteins, VLDL, Models, Biological, Triglycerides, Apolipoprotein A-I, Apolipoprotein C-II
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