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Genetic and epigenetic associations to obesity‐related appetite phenotypes among A frican– A merican children
Author(s) -
Gardner K. R.,
Sapienza C.,
Fisher J. O.
Publication year - 2015
Publication title -
pediatric obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.226
H-Index - 69
eISSN - 2047-6310
pISSN - 2047-6302
DOI - 10.1111/ijpo.12010
Subject(s) - epigenetics , appetite , medicine , obesity , dna methylation , childhood obesity , endocrinology , leptin , genetics , gene , biology , overweight , gene expression
Background Genetic and epigenetic variations may be an important contributer to altered eating behaviors in childhood which may lead to weight gain and obesity later in life. Objective This study aimed to evaluate epigenetic as well as genetic associations with appetite in young children. Subjects and methods Participants were 32 non‐obese and 32 obese A frican– A merican children aged 5–6 years. Saliva was collected from each child, and RNA and DNA were extracted for analysis. Individuals were genotyped for eating‐ and obesity‐associated single nucleotide polymorphisms in seven candidate genes ( FTO , MAOA , SH2B1 , LEPR , DNMT3B , BDNF and CCKAR ), and DNA methylation levels were measured in the upstream promoter region of each. Transcript levels of MAOA and FTO were also assessed. The Children's Eating Behavior Questionnaire ( CEBQ ) was used to assess the aspects of appetite. Child obesity was assessed using measured height and weight, and percent body fat was measured by dual‐energy X ‐ray absorptiometry. Results Food responsiveness was higher and satiety responsiveness was lower among obese than non‐obese female children ( P = 0.001 and P = 0.031), but did not differ among male children. Epigenetic analysis of the BDNF promoter revealed associations with altered satiety responsiveness among female children ( P < 0.01). Conclusion The findings provide new evidence of epigenetic associations with altered appetite among young A frican– A merican girls.