Association of the DNA Methylation of Obesity-Related Genes with the Dietary Nutrient Intake in Children

Nutrients. 2023 Jun 22;15(13):2840. doi: 10.3390/nu15132840.

Abstract

The occurrence of obesity stems from both genetic and external influences. Despite thorough research and attempts to address it through various means such as dietary changes, physical activity, education, and medications, a lasting solution to this widespread problem remains elusive. Nutrients play a crucial role in various cellular processes, including the regulation of gene expression. One of the mechanisms by which nutrients can affect gene expression is through DNA methylation. This modification can alter the accessibility of DNA to transcription factors and other regulatory proteins, thereby influencing gene expression. Nutrients such as folate and vitamin B12 are involved in the one-carbon metabolism pathway, which provides the methyl groups necessary for DNA methylation. Studies have shown that the inadequate intake of these nutrients can lead to alterations in DNA methylation patterns. For this study, we aim to understand the differences in the association of the dietary intake between normal weight and overweight/obese children and between European American and African American children with the DNA methylation of the three genes NRF1, FTO, and LEPR. The research discovered a significant association between the nutritional intake of 6-10-years-old children, particularly the methyl donors present in their diet, and the methylation of the NRF1, FTO, and LEPR genes. Additionally, the study emphasizes the significance of considering health inequalities, particularly family income and maternal education, when investigating the epigenetic impact of methyl donors in diet and gene methylation.

Keywords: DNA methylation; childhood obesity; dietary intake; epigenetics; folate intake; health disparities; methyl donors.

MeSH terms

  • Alpha-Ketoglutarate-Dependent Dioxygenase FTO / metabolism
  • Child
  • DNA Methylation*
  • Diet
  • Eating
  • Folic Acid / metabolism
  • Humans
  • Nutrients
  • Pediatric Obesity* / genetics

Substances

  • Folic Acid
  • FTO protein, human
  • Alpha-Ketoglutarate-Dependent Dioxygenase FTO

Grants and funding

This work was supported by the Alabama Agricultural Experiment Station and the Hatch Program of the National Institute of Food and Agriculture, US Department of Agriculture, to J.R.B. and T.G.