Dietary fat intake modifies the influence of the FTO rs9939609 polymorphism on adiposity in adolescents: The HELENA cross-sectional study

Carregando...
Imagem de Miniatura
Citações na Scopus
22
Tipo de produção
article
Data de publicação
2016
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCI LTD
Autores
LABAYEN, I.
RUIZ, J. R.
HUYBRECHTS, I.
ORTEGA, F. B.
ARENAZA, L.
GONZALEZ-GROSS, M.
WIDHALM, K.
MOLNAR, D.
MANIOS, Y.
DEHENAUW, S.
Citação
NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, v.26, n.10, p.937-943, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background and aims: The fat mass and obesity associated gene (FTO) has been associated with obesity and dietary intake. The aims were: (i) To assess whether energy and macro-nutrient intakes were different across the FTOrs9939609 genotypes in adolescents, and (ii) to explore whether dietary fat intake modified the association of the rs9939609 polymorphism with adiposity. Methods and results: The FTOrs9939609 polymorphism was genotyped in 652 adolescents (53% females, 14.8 +/- 1.2 years, TT = 246, TA = 296, AA = 110). Energy and macronutrient intake were assessed by two non-consecutive 24 h-recalls. Weight, height, waist circumference and skinfold thicknesses were measured and body fat percent was calculated. Energy and macronutrient intake were similar across the FTOrs9939609 genotypes (P > 0.2). There were significant interactions between the FTO polymorphism and fat intake on adiposity estimates (P < 0.05). In adolescents whose fat intake was below 30% (N =203), the A allele of rs9939609 was not associated with adiposity indices. In contrast, in adolescents whose fat intake was between 30% and 35% of energy (N = 190), the rs9939609 polymorphismwas associated with a 1.9% higher body fat per risk allele (95% CI: 0.39, 3.33; P < 0.05), and in those whose fat intake was higher than 35% (N =259), it was associated with a 2.8% higher body fat per risk allele (95% CI: 1.27, 4.43; P < 0.001). Conclusions: These findings support the concept that the deleterious effect of the FTOrs9939609 polymorphism on adiposity is exacerbated in adolescents consuming high fat diets. In contrast, the consumption of low fat diets (< 30% of energy) may attenuate the genetic predisposition to obesity in risk allele carriers.
Palavras-chave
FTO gene, Diet composition, Fat intake, Obesity, Adolescents
Referências
  1. Andreasen CH, 2008, DIABETES, V57, P95, DOI 10.2337/db07-0910
  2. Biro G, 2002, EUR J CLIN NUTR, V56, pS25, DOI 10.1038/sj/ejcn/1601426
  3. Black AE, 2000, INT J OBESITY, V24, P1119, DOI 10.1038/sj.ijo.0801376
  4. Black AE, 2000, EUR J CLIN NUTR, V54, P395, DOI 10.1038/sj.ejcn.1600971
  5. Burrows TL, 2010, J AM DIET ASSOC, V110, P1501, DOI 10.1016/j.jada.2010.07.008
  6. Cecil JE, 2008, NEW ENGL J MED, V359, P2558, DOI 10.1056/NEJMoa0803839
  7. Cole TJ, 2012, PEDIATR OBES, V7, P284, DOI [10.1111/j.2047-6310.2012.00064.x, 10.1111/j.2047-6310.2012.000064.x]
  8. Gustavsson J, 2016, EUR J NUTR, V55, P247, DOI 10.1007/s00394-015-0842-0
  9. Hardy DS, 2014, J AM COLL NUTR, V33, P256, DOI 10.1080/07315724.2013.879458
  10. Haubrock J, 2010, ARCH PUBLIC HLTH, V68, P14
  11. Johnson L, 2008, AM J CLIN NUTR, V87, P846
  12. Johnson L, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0004594
  13. Kilpelainen TO, 2011, PLOS MED, V8, DOI 10.1371/journal.pmed.1001116
  14. Labayen I, 2011, INT J OBESITY, V35, P66, DOI 10.1038/ijo.2010.219
  15. Labayen I, 2014, CLIN NUTR, V33, P859, DOI 10.1016/j.clnu.2013.10.008
  16. Labayen I, 2015, NUTR HOSP, V31, P2025, DOI 10.3305/nh.2015.31.5.8666
  17. Lappalainen T, 2012, BRIT J NUTR, V108, P1859, DOI 10.1017/S0007114511007410
  18. Lappalainen TJ, 2009, OBESITY, V17, P832, DOI 10.1038/oby.2008.618
  19. Liu GF, 2010, BMC MED GENET, V11, DOI 10.1186/1471-2350-11-57
  20. Livingstone KM, 2015, OBES REV, V16, P666, DOI 10.1111/obr.12290
  21. Livingstone MBE, 2003, EUR J CLIN NUTR, V57, P455, DOI 10.1038/sj.ejcn.1601563
  22. Loos RJF, 2005, J AM DIET ASSOC, V105, pS29, DOI 10.1016/j.jada.2005.02.015
  23. Loos RJF, 2014, NAT REV ENDOCRINOL, V10, P51, DOI 10.1038/nrendo.2013.227
  24. Moreno LA, 2008, INT J OBES LOND S, V5, pS4
  25. Nagy E, 2008, INT J OBES LOND S, V5, pS58
  26. Qi QB, 2014, HUM MOL GENET, V23, P6961, DOI 10.1093/hmg/ddu411
  27. Qi QB, 2015, DIABETES, V64, P2467, DOI 10.2337/db14-1629
  28. Rendo T, 2009, OBESITY FACTS, V2, P393, DOI 10.1159/000262296
  29. Rodriguez G, 2005, EUR J CLIN NUTR, V59, P1158, DOI 10.1038/sj.ejcn.1602226
  30. Ruiz JR, 2010, ARCH PEDIAT ADOL MED, V164, P328, DOI 10.1001/archpediatrics.2010.29
  31. Santos Luana C dos, 2010, J Pediatr (Rio J), V86, P400, DOI 10.2223/JPED.2025
  32. Schofield WN., 1958, HUM NUTR CLIN NUT S1, V39, P5
  33. Sonestedt E, 2009, AM J CLIN NUTR, V90, P1418, DOI 10.3945/ajcn.2009.27958
  34. Tanofsky-Kraff M, 2009, AM J CLIN NUTR, V90, P1483, DOI 10.3945/ajcn.2009.28439
  35. Timpson NJ, 2008, AM J CLIN NUTR, V88, P971
  36. Uauy R, 2009, ANN NUTR METAB, V55, P76, DOI 10.1159/000228997
  37. Vereecken CA, 2008, INT J OBES LOND S32, V5, pS26
  38. Vimaleswaran KS, 2012, OBESITY, V20, P1669, DOI 10.1038/oby.2012.49
  39. Zheng Y, 2015, J NUTR, V145, P977, DOI 10.3945/jn.115.210005