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  • Lai, Chao-QiangTufts Univ, USDA ARS, Nutr & Genom Lab, JM USDA Human Nutr Res Ctr, Boston, MA 02111 USA. (author)

Carbohydrate and fat intake associated with risk of metabolic diseases through epigenetics of CPT1A

  • Article/chapterEnglish2020

Publisher, publication year, extent ...

  • OXFORD UNIV PRESS,2020
  • printrdacarrier

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  • LIBRIS-ID:oai:DiVA.org:uu-429054
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-429054URI
  • https://doi.org/10.1093/ajcn/nqaa233DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Background: Epigenome-wide association studies identified the cg00574958 DNA methylation site at the carnitinc palmitoyltransferase-1A (CPT1A) gene to be associated with reduced risk of metabolic diseases (hypertriglyceridemia, obesity, type 2 diabetes, hypertension, metabolic syndrome). but the mechanism underlying these associations is unknown. Objectives: We aimed to elucidate whether carbohydrate and fat intakes modulate cg00574958 methylation and the risk of metabolic diseases. Methods: We examined associations between carbohydrate (CHO) and fat (FAT) intake, as percentages of total diet energy, and the CHO/FAT ratio with CPT1A-cg00574958, and the risk of metabolic diseases in 3 populations (Genetics of Lipid Lowering Drugs and Diet Network. n = 978; Framingham Heart Study. n = 2331: and REgistre GIroni del COR study, n = 645) while adjusting for confounding factors. To understand possible causal effects of dietary intake on the risk of metabolic diseases, we performed metaanalysis, CPT1A transcription analysis, and mediation analysis with CHO and FAT intakes as exposures and cg00574958 methylation as the mediator. Results: We confirmed strong associations of cg00574958 methylation with metabolic phenotypes (BMI, triglyceride, glucose) and diseases in all 3 populations. Our results showed that CHO intake and CHO/FAT ratio were positively associated with cg00574958 methylation. whereas FAT intake was negatively correlated with cg00574958 methylation. Meta-analysis further confirmed this strong correlation, with beta = 58.4 +/- 7.27, P = 8.98 x 10(-16) for CHO intake; beta = -36.4 +/- 5.95. P = 9.96 x 10(-10) for FAT intake; and beta = 3.30 +/- 0.49. P = 1.48 x 10(-11) for the CHO/FAT ratio. Furthermore, CPT1A mRNA expression was negatively associated with CHO intake, and positively associated with FAT intake, and metabolic phenotypes. Mediation analysis supports the hypothesis that CHO intake induces CPT1A methylation, hence reducing the risk of metabolic diseases, whereas FAT intake inhibits CPT1A methylation, thereby increasing the risk of metabolic diseases. Conclusions: Our results suggest that the proportion of total energy supplied by CHO and FAT can have a causal effect on the risk of metabolic diseases via the epigenetic status of CPT1A.

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  • Parnell, Laurence D.Tufts Univ, USDA ARS, Nutr & Genom Lab, JM USDA Human Nutr Res Ctr, Boston, MA 02111 USA. (author)
  • Smith, Caren E.Tufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA. (author)
  • Guo, TaoTufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA. (author)
  • Sayols-Baixeras, SergiUppsala universitet,Molekylär epidemiologi,IMIM Hosp del Mar Med Res Inst, Cardiovasc Epidemiol & Genet Res Grp, Barcelona, Catalonia, Spain.;CIBER Cardiovasc Dis CIBERCV, Barcelona, Catalonia, Spain(Swepub:uu)sersa467 (author)
  • Aslibekyan, StellaUniv Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA. (author)
  • Tiwari, Hemant K.Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA. (author)
  • Irvin, Marguerite R.Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA. (author)
  • Bender, CarlTufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA. (author)
  • Fei, DavidTufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA. (author)
  • Hidalgo, BerthaUniv Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA. (author)
  • Hopkins, Paul N.Univ Utah, Dept Cardiovasc Genet, Salt Lake City, UT USA. (author)
  • Absher, Devin M.Hudson Alpha Inst Biotechnol, Huntsville, AL USA. (author)
  • Province, Michael A.Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA. (author)
  • Elosua, RobertoIMIM Hosp del Mar Med Res Inst, Cardiovasc Epidemiol & Genet Res Grp, Barcelona, Catalonia, Spain.;CIBER Cardiovasc Dis CIBERCV, Barcelona, Catalonia, Spain. (author)
  • Arnett, Donna K.Univ Kentucky, Coll Publ Hlth, Lexington, KY USA. (author)
  • Ordovas, Jose M.Tufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA.;CEI UAM CSIC, IMDEA Food Inst, Madrid, Spain.;Ctr Nacl Invest Cardiovasc CNIC, Madrid, Spain. (author)
  • Tufts Univ, USDA ARS, Nutr & Genom Lab, JM USDA Human Nutr Res Ctr, Boston, MA 02111 USA.Tufts Univ, JM USDA Human Nutr Res Ctr Aging, Nutr & Genom Lab, Boston, MA 02111 USA. (creator_code:org_t)

Related titles

  • In:American Journal of Clinical Nutrition: OXFORD UNIV PRESS112:5, s. 1200-12110002-91651938-3207

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