N-3 fatty acids stimulate intracellular degradation of apoprotein B in rat hepatocytes.
Open accessAbstract
When rat hepatocytes were incubated with albumin complexed to the n-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), rather than to oleic acid (OA), the secretion of newly synthesized apoprotein B100 (apoB100) or B48 (apoB48) was reduced, despite stimulation of cellular triglyceride synthesis by all three fatty acids. When pulse-chase studies of apoB synthesis and secretion were performed in the presence of OA, EPA, or DHA, there were no significant changes in the initial synthetic rates of either apoB species. However, during the chase period, the total recovery of labeled apoB100 and apoB48 from the cell and medium was less in the n-3 fatty acid groups, so that by 150 min, approximately half as much labeled apoB was recovered as in the OA group. Overall, the decreased accumulation in medium of labeled apoB in the presence of EPA and DHA could be quantitatively accounted for by increased degradation of intracellular apoB. Thus, in the primary hepatocyte, apoB degradation is not constitutive, but can be regulated by n-3 fatty acids.
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Omega-3 fatty acids lead to intracellular degradation of apo B, thereby diminishing VLDL assembly and decreasing VLDL secretion.
“In addition, n-3 FAs lead to intracellular degradation of apo B, which may be a result of decreased triglyceride availability or autophagic destruction of apo B via post-Golgi oxidation, 90 thereby diminishing the assembly of VLDL particles in the hepatocyte and decreasing VLDL secretion.91,92”
From Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association (2019) · cites this paper as [92]
The Abstract and the discussion on p. 1387 report that EPA and DHA increased intracellular apoB degradation in rat hepatocytes, accounting for decreased secretion of newly synthesized apoB. The paper does not establish that degradation thereby diminishes VLDL assembly; on p. 1387 it treats interference with assembly as a possible cause of apoB degradation, rather than a demonstrated consequence. (LLM, conf=0.86)
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Self-citation
- Authors
- Wang, H., Chen, X., & Fisher, E. A.
- ORCID
- Fisher, E A
- Venue
- Journal of Clinical Investigation
- Published
- 1993-04-01
- Volume
- 91
- Issue
- 4
- Pages
- 1380-1389
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC288110
- OpenAlex
- W2125790654
- Cited by
- 133
- References
- 44
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 5 · 2012: 7
- FWCI
- 12.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- W. W. Smith Charitable Trust
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL22633, P01HL022633)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- omega-3 fatty acids, eicosapentaenoic acid, docosahexaenoic acid, oleic acid, apolipoprotein B-100, apolipoprotein B-48, intracellular protein degradation, hepatocytes, triglyceride synthesis, lipoprotein secretion
- MeSH terms
- Animals, Apolipoproteins B, Cells, Cultured, Chemistry, Physical, Cycloheximide, Docosahexaenoic Acids, Kinetics, Liver, Precipitin Tests, Protein Denaturation, RNA, Messenger, Eicosapentaenoic Acid, Fatty Acids, Omega-3, Rats, Chemical Phenomena
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