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

Author:

Liu Ruyu1ORCID,Hannon Bridget A1,Robinson Katie N1,Raine Lauren B2,Hammond Billy R3,Renzi-Hammond Lisa M34,Cohen Neal J567,Kramer Arthur F26,Hillman Charles H28,Teran-Garcia Margarita19,Khan Naiman A110ORCID

Affiliation:

1. Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA

2. Department of Psychology, Northeastern University, Boston, MA, USA

3. Department of Psychology, University of Georgia, Athens, GA, USA

4. College of Public Health, Institute of Gerontology, University of Georgia, Athens, GA, USA

5. Department of Psychology, University of Illinois at Urbana-Champaign, Urbana, IL, USA

6. Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, IL, USA

7. Center for Nutrition, Learning, and Memory, University of Illinois at Urbana-Champaign, Urbana, IL, USA

8. Department of Physical Therapy, Movement, & Rehabilitation Sciences, Northeastern University, Boston, MA, USA

9. Department of Human Development and Family Studies, University of Illinois at Urbana-Champaign, Urbana, IL, USA

10. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, IL, USA

Abstract

ABSTRACT 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 β-carotene-15,15′-monooxygenase (BCO1)-rs7501331 (T allele) (P = 0.045), cluster of differentiation 36(CD36)-rs1527483 (T 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 BCO1 contribute to MPOD in children. The influence of genetic variation in CD36-rs3173798 persisted after adjusting for variation in dietary intake. This trial was registered at clinicaltrials.gov as NCT01619826.

Funder

NIH

Abbott Nutrition

Center for Nutrition, Learning, and Memory

USDA

National Institute of Food and Agriculture

Agriculture and Food Research Initiative Competitive

Cooperative Extension

Department of Human Development and Family Studies

University of Illinois at Urbana-Champaign

Publisher

Oxford University Press (OUP)

Subject

Nutrition and Dietetics,Medicine (miscellaneous)

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