4.6 Article

Single Nucleotide Polymorphisms in CD36 Are Associated with Macular Pigment among Children

期刊

JOURNAL OF NUTRITION
卷 151, 期 9, 页码 2533-2540

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jn/nxab153

关键词

lutein; zeaxanthin; macular pigment optical density; nutrigenetics; pediatric; carotenoids

资金

  1. NIH [HD069381]
  2. Abbott Nutrition grant through the Center for Nutrition, Learning, and Memory [2012-04608]
  3. USDA National Institute of Food and Agriculture (NIFA) [2011-67001-30101]
  4. Agriculture and Food Research Initiative Competitive Grant from the USDA NIFA [2015-68001-23248]
  5. University of Illinois at UrbanaChampaign

向作者/读者索取更多资源

The study found that specific genetic variations, such as in BCO1 and CD36, are associated with lower levels of MPOD in children. The impact of genetic variation in CD36-rs3173798 on MPOD persisted even after adjusting for dietary intake.
Background: High macular pigment optical density (MPOD) has been associated with improved eye health and better cognitive functions. Genetic variations have been associated with MPOD in adults. However, these associations between genetic variations and MPOD have not been studied in children. Objectives: This was a secondary analysis of the FK2 (Fitness Improves Thinking in Kids 2) trial (n = 134, 41% male). The aim was to determine differences in MPOD among children (aged 7-9 y) based on genetic variants that either are biologically relevant to lutein (L) and zeaxanthin (Z) accumulation or have been associated with MPOD in adults. Methods: MPOD was measured using customized heterochromatic flicker photometry via a macular densitometer. DXA was used to assess whole-body and visceral adiposity. DNA was extracted from saliva samples and was genotyped for 26 hypothesis-driven single nucleotide polymorphisms and 75 ancestry-informative markers (AIMs). Habitual diet history was obtained via 3-d food logs completed by parents (n = 88). General linear models were used to compare MPOD between different genotypes. Principal component analysis was performed for the AIMs to account for ethnic heterogeneity. Results: Children carrying >= 1 minor allele on beta-carotene-15,15'-monooxygenase (BCO1-rs7501331 IT allele) (P= 0.045), cluster of differentiation 36 (CD36)-rs1527483 IT allele) (P= 0.038), or CD36-rs3173798 (C allele) (P= 0.001) had significantly lower MPOD (range: 14.1%-26.4%) than those who were homozygotes for the major alleles. MPOD differences based on CD36-rs3173798 genotypes persisted after adjustment for dietary L and Z intake. Conclusions: The findings indicate that genetic variations of CD36 and BC01 contribute to MPOD in children. The influence of genetic variation in CD36-rs3173798 persisted after adjusting for variation in dietary intake.

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