APOC3 Promoter Polymorphisms C-482T and T-455C Are Associated with the Metabolic Syndrome
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Background Despite the growing epidemic of the metabolic syndrome (MetS), few studies have evaluated genetic polymorphisms associated with the MetS phenotype. One candidate, APOC3, modulates lipid and lipoprotein metabolism and the promoter polymorphisms C-482T/T-455C are associated with loss of insulin downregulation.Methods One hundred twenty two consecutive MetS cases were matched by age, sex and race in a 1:1 case-control design to evaluate the prevalence of common polymorphisms in the following candidate genes: APOC3, APOE, B3AR, FABP2, GNB3, LPL, and PPARalpha and PPARgamma.Results Compared to controls, MetS subjects exhibited a greater prevalence of APOC3 promoter polymorphisms. Specifically, the frequency of the variant C-482T and T-455C alleles was 70.5 and 81.9% of cases compared to 43.4 and 54.1% in controls, respectively (p <0.0001). Overall, APOC3 promoter variants were associated with a greater likelihood of MetS compared to wild type [C-482T (OR: 4.3; 95% CI: 2.2, 8.6 [p <0.0001]), T-455C (OR: 3.6; 95% CI: 2.0, 6.7 [p <0.0001])]. No material differences were identified between the other genetic variants tested and prevalence of MetS.Conclusions These data, therefore, suggest that the APOC3 promoter polymorphisms C-482T and T-455C are associated with the MetS.
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Previous studies have suggested that two single-nucleotide polymorphisms in the gene encoding apolipoprotein C3 (APOC3) may be associated with hypertriglyceridemia.
“Previous studies have suggested that two single-nucleotide polymorphisms (SNPs) in the gene encoding apolipoprotein C3 (APOC3) may be associated with hypertriglyceridemia.4–8”
From Apolipoprotein C3 gene variants in nonalcoholic fatty liver disease (2010) · cites this paper as [8]
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References 55 · Cited by 89
- Authors
- Miller, M., Rhyne, J., Chen, H., Beach, V., Ericson, R., Luthra, K., Dwivedi, M., & Misra, A.
- Affiliations
- Baltimore VA Medical Center (US)
- All India Institute of Medical Sciences (IN)
- Corresponding author
- Miller, Michael
- Venue
- Archives of Medical Research
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 38
- Issue
- 4
- Pages
- 444-451
- ISSN
- 0066-6769 (ISSN-L)
- 0188-4409
- PMC
- PMC1987381
- OpenAlex
- W2136981300
- Cited by
- 89
- References
- 55
- Citations by year
- 2026: 1 · 2025: 4 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 5 · 2019: 1 · 2018: 2 · 2017: 6 · 2016: 6 · 2015: 7 · 2014: 6 · 2013: 9 · 2012: 5
- FWCI
- 5.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Archives of Medical Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs
- University of Delhi
- National Heart, Lung, and Blood Institute (HL061369, R01HL061369)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
- Keywords
- apolipoprotein C-III, promoter polymorphism, metabolic syndrome, genetic susceptibility, lipoprotein metabolism, insulin resistance, candidate genes, apolipoprotein E, FABP2, GNB3, lipoprotein lipase, PPARγ
- MeSH terms
- Adult, Female, Humans, Male, Middle Aged, Polymorphism, Genetic, Promoter Regions, Genetic, Genetic Predisposition to Disease, Metabolic Syndrome, Apolipoprotein C-III
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