Erin Kinnally; Jefferson Hunter; John Capitanio; Erika Jones; Elizabeth Wood, Brigham Young University
Obesity and body mass index (BMI) rates in the United States have increased substantially over the last few decades, elevating the risk for diabetes, heart disease, and other chronic health conditions. Many factors are believed to influence the increasing rate of obesity, including a number genomic components. While studies have investigated genomic factors contributing to weight their influence remains unclear. Due to the difficulty in controlling the human environment, which studies show to have a critical impact on genetic expression, translational animal models are useful in assessing genomic, and particularly epigenomic, contributions to development., This study will use a rhesus macaque (Macaca mulatta) model to address epigenetic (genome-wide DNA methylation patterns) contributions to weight gain. We will investigate methylation ratios in nine orthologues of genes associated with weight gain in humans (PEG3, FTO, IGF-2, VDR, CYP27B1, AGRP, LEP, MC4). The functions of these genes relate to appetite regulation (AGRP, LEP, MC4), cell and body growth (FTO, VDR, CYP27B1, PEG3) as well as metabolism (IGF-2). To do so, body weight of 154 infant rhesus monkeys was collected at 3-4 months of age. Blood was obtained and DNA was extracted. Restricted representation bisulfite sequencing of the nine genes was conducted and regions rich in cytosine-guanine pairs (CpG) islands were targeted upstream from the promoter region as a means of assessing the relative methylation of nucleotides. Methylation percentages of nucleotides were collected to determine likelihood of silence gene expression. Preliminary analyses show groupings of CpG islands in noncoding areas upstream from the promoter region. Linear regression will be used to assess the relationship between methylation magnitude in these nine genes and weight gain across development.