The association between APOA5 haplotypes and plasma lipids is not modified by energy or fat intake: the Czech HAPIEE study
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R01 AG023522
NIA NIH HHS - United States
R01 AG23522-01
NIA NIH HHS - United States
081081
Wellcome Trust - United Kingdom
064947
Wellcome Trust - United Kingdom
PubMed
24462044
PubMed Central
PMC4357849
DOI
10.1016/j.numecd.2013.08.008
PII: S0939-4753(13)00199-3
Knihovny.cz E-zdroje
- Klíčová slova
- Apolipoprotein A5, Interaction, Polymorphism, Total energy intake, Triglycerides,
- MeSH
- alely MeSH
- apolipoprotein A-V MeSH
- apolipoproteiny A genetika MeSH
- běloši MeSH
- cholesterol krev MeSH
- dietní tuky aplikace a dávkování MeSH
- energetický příjem * MeSH
- haplotypy * MeSH
- hodnocení stavu výživy MeSH
- index tělesné hmotnosti MeSH
- jednonukleotidový polymorfismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- lineární modely MeSH
- průzkumy a dotazníky MeSH
- senioři MeSH
- triglyceridy krev MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- APOA5 protein, human MeSH Prohlížeč
- apolipoprotein A-V MeSH
- apolipoproteiny A MeSH
- cholesterol MeSH
- dietní tuky MeSH
- triglyceridy MeSH
BACKGROUND AND AIMS: Several smaller studies reported interactions between dietary factors and apolipoprotein A5 (APOA5) gene polymorphisms in determination of plasma lipids. We tested interactions between APOA5 haplotypes and dietary intake in determination of plasma triglycerides (TG) and other lipids. METHODS AND RESULTS: Participants (5487 males and females aged 45-69) were classified according to the number (0, 1, 2+) of minor APOA5 alleles (using T-1131 > C; rs662799 and Ser19 > Trp; rs3135506 polymorphisms) and into three groups of low (bottom 25%), medium (26th-75th percentile) and high (top 25%) of intake of total energy and total, saturated and polyunsaturated fats, assessed by food frequency questionnaire. The age-sex adjusted geometric means of plasma TG increased with the number of minor alleles, from 1.57 (standard error 0.01), to 1.79 (0.02) to 2.29 (0.10) mmol/L (p < 0.00001) but TG did not differ between groups with low, medium and high total energy intake (p = 0.251). TG concentrations were highest in subjects with the combination of 2+ minor alleles and the highest energy intake (mean 2.59 [0.19], compared with 1.62 [0.03] in subjects with lowest energy intake and no minor allele) but the interaction between energy intake and APOA5 haplotypes was not statistically significant (p = 0.186). Analogous analyses with total, saturated and polyunsaturated fat intake yielded similar nonsignificant results. Effects of APOA5 and dietary intakes on total and HDL cholesterol were weaker and no interactions were significant. CONCLUSION: In this Slavic Caucasian population sample, we did not detect the hypothesized interaction between common SNPs within the APOA5 gene and diet in determination of blood lipids.
Zobrazit více v PubMed
Forrester J.S. Triglycerides: risk factor or fellow traveler? Curr Opin Cardiol. 2001;16:261–264. PubMed
Pennacchio L.A., Olivier M., Hubacek J.A., Cohen J.C., Cox D.R., Fruchart J.C., et al. An apolipoprotein influencing triglycerides in humans and mice revealed by comparative sequencing. Science. 2001;294:169–173. PubMed
Triglyceride Coronary Disease Genetics Consortium and Emerging Risk Factors Collaboration. Sarwar N., Sandhu M.S., Ricketts S.L., Butterworth A.S., Di Angelantonio E., Boekholdt S.M., et al. Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies. Lancet. 2010;375:1634–1639. PubMed PMC
Fruchart-Najib J., Bauge E., Niculescu L.S., Pham T., Thomas B., Rommens C., et al. Mechanism of triglyceride lowering in mice expressing human apolipoprotein A5. Biochem Biophys Res Commun. 2004;319:397–404. PubMed
Schaap F.G., Rensen P.C., Voshol P.J., Vrins C., van der Vliet H.N., Chamuleau R.A., et al. ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglyceride (VLDL-TG) production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis. J Biol Chem. 2004;279:27941–27947. PubMed
Dorfmeister B., Zeng W.W., Dichlberger A., Nilsson S.K., Schaap F.G., Hubacek J.A., et al. Effects of six APOA5 variants, identified in patients with severe hypertriglyceridemia, on in vitro lipoprotein lipase activity and receptor binding. Arterioscler Thromb Vasc Biol. 2008;28:1866–1871. PubMed
Pennacchio L.A., Olivier M., Hubacek J.A., Krauss R.M., Rubin E.M., Cohen J.C. Two independent apolipoprotein A5 haplotypes influence human plasma triglyceride levels. Hum Mol Genet. 2002;11:3031–3038. PubMed
Hubacek J.A. Apolipoprotein A5 and triglyceridemia. Focus on the effects of the common variants. Clin Chem Lab Med. 2005;43:897–902. PubMed
Hubacek J.A., Skodova Z., Adamkova V., Lanska V., Poledne R. The influence of APOAV polymorphisms (T-1131 > C and S19 > W) on plasma triglyceride levels and risk of myocardial infarction. Clin Genet. 2004;65:126–130. PubMed
Tai E.S., Ordovas J.M. Clinical significance of apolipoprotein A5. Curr Opin Lipidol. 2008;19:349–354. PubMed PMC
Jang Y., Chae J.S., Kim O.Y., Park H.J., Kim J.Y., Paik J.K., et al. APOA5-1131T > C genotype effects on apolipoprotein A5 and triglyceride levels in response to dietary intervention and regular exercise (DIRE) in hypertriglyceridemic subjects. Atherosclerosis. 2010;211:512–519. PubMed
Lin J., Fang D.Z., Du J., Shigdar S., Xiao L.Y., Zhou X.D., et al. Elevated levels of triglyceride and triglyceride-rich lipoprotein triglyceride induced by a high-carbohydrate diet is associated with polymorphisms of APOA5-1131T > C and APOC3-482C > T in Chinese healthy young adults. Ann Nutr Metab. 2011;58:150–157. PubMed
Kim J.Y., Kim O.Y., Koh S.J., Jang Y., Yun S.S., Ordovas J.M., et al. Comparison of low-fat meal and high-fat meal on postprandial lipemic response in non-obese men according to the -1131T > C polymorphism of the apolipoprotein A5 (APOA5) gene (randomized cross-over design) J Am Coll Nutr. 2006;25:340–347. PubMed
Zhang X., Qi Q., Bray G.A., Hu F.B., Sacks F.M., Qi L. APOA5 genotype modulates 2-y changes in lipid profile in response to weight-loss diet intervention: the Pounds Lost Trial. Am J Clin Nutr. 2012;96:917–922. PubMed PMC
Lai C.Q., Corella D., Demissie S., Cupples L.A., Adiconis X., Zhu Y., et al. Dietary intake of n-6 fatty acids modulates effect of apolipoprotein A5 gene on plasma fasting triglycerides, remnant lipoprotein concentrations, and lipoprotein particle size: the Framingham Heart Study. Circulation. 2006;113:2062–2070. PubMed
Mattei J., Demissie S., Tucker K.L., Ordovas J.M. Apolipoprotein A5 polymorphisms interact with total dietary fat intake in association with markers of metabolic syndrome in Puerto Rican older adults. J Nutr. 2009;139:2301–2308. PubMed PMC
Marques-Vidal P., Arveiler D., Evans A., Amouyel P., Ferrieres J., Ducimetiere P. Different alcohol drinking and blood pressure relationships in France and Northern Ireland: the PRIME Study. Hypertension. 2001;38:1361–1366. PubMed
Peasey A., Bobak M., Kubinova R., Malyutina S., Pajak A., Tamosiunas A., et al. Determinants of cardiovascular disease and other non-communicable diseases in Central and Eastern Europe: rationale and design of the HAPIEE study. BMC Public Health. 2006;18:255. www.biomedcentral.com/1471-2458/6/255 PubMed PMC
Willett W.C., Sampson L., Stampfer M.J., Rosner B., Bain C., Witschi J., et al. Reproducibility and validity of a semiquantitative food frequency questionnaire. Am J Epidemiol. 1985;122:51–65. PubMed
Brunner E., Stallone D., Juneja M., Bingham S., Marmot M. Dietary assessment of Whitehall II: comparison of 7-day diet diary and food frequency questionnaire and validity against biomarkers. Br J Nutr. 2001;85:405–414. PubMed
McCance R., Widdowson E. Royal Statistical Society; Cambridge: 2002. McCance & Widdowson's the composition of foods: summary edition.
Boylan S., Welch A., Pikhart H., Malyutina S., Pajak A., Kubinova R., et al. Dietary habits in three Central and Eastern European countries: the HAPIEE study. BMC Public Health. 2009;9:439. PubMed PMC
Krauss R.M. Dietary and genetic probes of atherogenic dyslipidemia. Arterioscler Thromb Vasc Biol. 2005;25:2265–2272. PubMed
Fenech M., El-Sohemy A., Cahill L., Ferguson L.R., French T.A., Tai E.S., et al. Nutrigenetics and nutrigenomics: viewpoints on the current status and applications in nutrition research and practice. J Nutrigenet Nutrigenomics. 2011;4:69–89. PubMed PMC
Garcia-Rios A., Perez-Martinez P., Delgado-Lista J., Lopez-Miranda J., Perez-Jimenez F. Nutrigenetics of the lipoprotein metabolism. Mol Nutr Food Res. 2012;56:171–183. PubMed
Hubacek J.A., Skodova Z., Adamkova V., Lanska V., Pitha J. APOA5 variant Ser19Trp influences a decrease of the total cholesterol in a male 8 year cohort. Clin Biochem. 2006;39:133–136. PubMed
Hubacek J.A., Bohuslavova R., Skodova Z., Pitha J., Bobkova D., Poledne R. Polymorphisms in the APOA1/C3/A4/A5 gene cluster and cholesterol responsiveness to dietary change. Clin Chem Lab Med. 2007;45:316–320. PubMed
Paula R.S., Souza V.C., Benedet A.L., Souza E.R., Toledo J.O., Moraes C.F., et al. Dietary fat and apolipoprotein genotypes modulate plasma lipoprotein levels in Brazilian elderly women. Mol Cell Biochem. 2010;337:307–315. PubMed
Sanchez-Moreno C., Ordovas J.M., Smith C.E., Baraza J.C., Lee Y.C., Garaulet M. APOA5 gene variation interacts with dietary fat intake to modulate obesity and circulating triglycerides in a Mediterranean population. J Nutr. 2011;141:380–385. PubMed PMC