The DOI matches its Crossref record; 69 of the 70 references it cites were found in a registry or an index.
ApoE Polymorphism and Fish Oil Supplementation in Subjects With an Atherogenic Lipoprotein Phenotype
Open accessAbstract
Abstract —The study assessed the efficacy of fish oil supplementation in counteracting the classic dyslipidemia of the atherogenic lipoprotein phenotype (ALP). In addition, the impact of the common apolipoprotein E (apoE) polymorphism on the fasting and postprandial lipid profile and on responsiveness to the dietary intervention was established. Fifty-five ALP males (aged 34 to 69 years, body mass index 22 to 35 kg/m 2 , triglyceride [TG] levels 1.5 to 4.0 mmol/L, high density lipoprotein cholesterol [HDL-C] <1.1 mmol/l, and percent low density lipoprotein [LDL]-3 >40% total LDL) completed a randomized placebo-controlled crossover trial of fish oil (3.0 g eicosapentaenoic acid/docosahexaenoic acid per day) and placebo (olive oil) capsules with the 6-week treatment arms separated by a 12-week washout period. In addition to fasting blood samples, at the end of each intervention arm, a postprandial assessment of lipid metabolism was carried out. Fish oil supplementation resulted in a reduction in fasting TG level of 35% ( P <0.001), in postprandial TG response of 26% (TG area under the curve, P <0.001), and in percent LDL-3 of 26% ( P <0.05). However, no change in HDL-C levels was evident ( P =0.752). ANCOVA showed that baseline HDL-C levels were significantly lower in apoE4 carriers ( P =0.035). The apoE genotype also had a striking impact on lipid responses to fish oil intervention. Individuals with an apoE2 allele displayed a marked reduction in postprandial incremental TG response (TG incremental area under the curve, P =0.023) and a trend toward an increase in lipoprotein lipase activity relative to non-E2 carriers. In apoE4 individuals, a significant increase in total cholesterol and a trend toward a reduction in HDL-C relative to the common homozygous E3/E3 profile was evident. Our data demonstrate the efficacy of fish oil fatty acids in counteracting the proatherogenic lipid profile of the ALP but also that the apoE genotype influences responsiveness to this dietary treatment.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“Although most trials presented in Table 4 specified direct LDL-C measurement in cases when triglycerides >400 mg/dL (as is standard for clinical practice), only 3 trials reported LDL-C results obtained from direct LDL measurement throughout the triglyceride range.28,30,45”
From Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association (2019) · cites this paper as [45]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“On average, the triglyceride reduction was ≈27% (range, 21%-35%), apart from the study of a medical food (3.2 g/d EPA+DHA), which specifically recruited people with very low blood levels of n-3 FA and reported a 48% reduction.”
From Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association (2019) · cites this paper as [45]
Experimental — accuracy not yet measuredIn the citing paper
“Total cholesterol levels increased in APOE4 carriers and, although not statistically significant, LDL-C levels tended to increase more in APOE4 carriers than in APOE2 or APOE3 carriers following OM3FA treatment.”
In the citing paper
“However, small dense LDL levels decreased similarly in the different APOE genotypes [59].”
In the citing paper
“Minihane et al. were the first to show that the effect of OM3FAs on LDL was dependent on APOE genotype [59].”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
A SIMPLE METHOD FOR THE ISOLATION AND PURIFICATION OF TOTAL LIPIDES FROM ANIMAL TISSUES
Folch, J., Lees, M., & Stanley, G. H. S. (1957) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)64849-5 · Cited by 65,189
Friedewald, W. T., Levy, R. I., & Fredrickson, D. S. (1972) · Clinical Chemistry · doi:10.1093/clinchem/18.6.499 · Cited by 32,423
The Metabolic Basis of Inherited Disease.
(1988) · Annals of Internal Medicine · doi:10.7326/0003-4819-108-3-503_7 · Cited by 7,807
Apolipoprotein E polymorphism and atherosclerosis.
Davignon, J., Gregg, R. E., & Sing, C. F. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.1.1 · Cited by 1,981
Low-Density Lipoprotein Subclass Patterns and Risk of Myocardial Infarction
Austin, M. A. (1988) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.1988.03410130125037 · Cited by 1,780
Hokanson, J. E., & Austin, M. A. (1996) · Journal of Cardiovascular Risk · doi:10.1097/00043798-199604000-00014 · Cited by 1,706
Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk
Austin, M. A., King, M. C., Vranizan, K. M., & Krauss, R. M. (1990) · Circulation · doi:10.1161/01.cir.82.2.495 · Cited by 1,411
n-3 fatty acids and serum lipoproteins: human studies
Harris, W. (1997) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/65.5.1645s · Cited by 1,243
Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review
Harris, W. S. (1989) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38310-3 · Cited by 1,127
Lipolytic Enzymes and Plasma Lipoprotein Metabolism
Nilsson‐Ehle, P., Garfinkel, A. S., & Schotz, M. C. (1980) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.49.070180.003315 · Cited by 754
Flagged first, then by citations
1 of the 70 references couldn’t be matched to a known paper.
Research works printed but not linked: 18
- 10.1161/atv91.11.1.1987999 · DOI
- 1994, Atherosclerosis, 197, 106
- 10.1161/atv91.14.11.7947602 · DOI
- 10.1161/circ.82.2.2372896 · DOI
- 1988, JAMA, 260, 917
- 1980, Trans Assoc Am Physicians, 43, 148
- 1988, J Clin Invest, 82, 1844
- 1988, J Lipid Res, 299, 1451
- 1994, Am J Hum Genet, 54, 341
- 10.1161/atv91.11.6.1931875 · DOI
- 1995, Clin Chem, 4, 1599
- 1986, J Lipid Res, 27, 227
- 1986, J Clin Invest, 11, 1303
- 10.1161/atvb.17.9.1675 · DOI
- 1984, J Clin Invest, 74, 72
- 1994, Eur J Clin Nutr, 48, 26
- Minihane AM Khan S Talmud PJ Williams DL Wright JW Murphy MC Griffin BA Williams CM. In subjects with an atherogenic lipoprotein phenotype (ALP) central adiposity is associated with an attenuated postprandial triglyceride response. Int J Obes. In press.
- 10.1161/atv91.13.12.8241095 · DOI
Cited by
Sorted by citations
Items 201–215 of 215
Differences in transcriptional responses to acute and chronic dietary interventions with fatty acids
Matualatupauw, J. C. (2017) · doi:10.18174/414660
Caron‐Dorval, D. (2014) · Corpus Université Laval (Université Laval)
(2018) · Wiley eBooks · doi:10.1002/9781118829875.refs
Cognitive decline and Alzheimer’s disease
Leray, C. (2017) · CRC Press eBooks · doi:10.1201/9781315268828-5
Meyer, B. J. (2018) · MDPI eBooks · doi:10.3390/books978-3-03842-972-2
Ozen, E., Mihaylova, R., Lord, N., Lovegrove, J. A., & Jackson, K. G. (2022) · Proceedings of The Nutrition Society · doi:10.1017/s0029665122000283
(2005) · Wiley eBooks · doi:10.1002/9780470774663.refs
(2001) · Proceedings of The Nutrition Society · doi:10.1017/s0029665101000623
Harris, W. S., & Jacobson, T. A. (2015) · Elsevier eBooks · doi:10.1016/b978-0-323-28786-9.00026-8
SUBCLINICAL CARDIOVASCULAR DISEASE AND ITS ASSOCIATED RISK FACTORS IN DIFFERENT POPULATION GROUPS
Choo, J. (2008) · D-Scholarship@Pitt (University of Pittsburgh)
ApoE, Obesity, and Metabolic Syndrome
Carvalho-Rassbach, M., & ALVAREZ-LEITE, J. I. (2025) · Springer eBooks · doi:10.1007/978-3-031-52641-1_27-1
de Almeida, R. M., Giannetti, W. D., Silveira, G. R., Castilho, C. R., Lisboa, R. V., Ciambarella, B. T., Ferreira, R. N., & de Carvalho, J. J. (2024) · Journal of Biosciences and Medicines · doi:10.4236/jbm.2024.125017
ApoE, Obesity, and Metabolic Syndrome
Carvalho-Rassbach, M., & ALVAREZ-LEITE, J. I. (2026) · Springer eBooks · doi:10.1007/978-3-031-96089-5_27
APOB to Estimated APOB Ratio for Screening for the APOE2 Genotype
Auger, C., Sampson, M. L., Zubirán, R., Cole, J., Wolska, A. T., Otvos, J. D., Sniderman, A. D., & Remaley, A. T. (2026) · Clinical Chemistry · doi:10.1093/clinchem/hvag094
Traczyk, I. (2013) · Żywienie Człowieka i Metabolizm
Metadata
- Authors
- Minihane, A. M., Khan, S., Leigh-Firbank, E. C., Talmud, P., Wright, J. W., Murphy, M. C., Griffin, B. A., & Williams, C. M.
- Affiliations
- University of Surrey (GB)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2000-08
- Volume
- 20
- Issue
- 8
- Pages
- 1990-1997
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2133738729
- Cited by
- 215
- References
- 70
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 5 · 2021: 8 · 2020: 4 · 2019: 8 · 2018: 6 · 2017: 13 · 2016: 7 · 2015: 5 · 2014: 12 · 2013: 12 · 2012: 12
- FWCI
- 7.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- UEA Digital Repository (University of East Anglia) (submittedVersion)
- Funders
- Directorate for Biological Sciences
- Biotechnology and Biological Sciences Research Council
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- APOE polymorphism, fish oil supplementation, eicosapentaenoic acid, docosahexaenoic acid, atherogenic lipoprotein phenotype, dyslipidemia, postprandial triglyceride response, HDL cholesterol, LDL cholesterol, lipoprotein lipase activity, APOE ε4 carriers, ApoE2 allele, olive oil placebo
- MeSH terms
- Adult, Aged, Apolipoproteins E, Arteriosclerosis, Double-Blind Method, Fasting, Fatty Acids, Nonesterified, Fish Oils, Food, Genotype, Humans, Lipoproteins, Cholesterol, HDL, Cholesterol, LDL, Male, Middle Aged, Phenotype, Placebos, Polymorphism, Genetic, Triglycerides, Cross-Over Studies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
