1Department of Anthropology, Western Washington University, 2School of Biosciences, University of Nottingham, 3Department of Forensic Sciences, George Washington University
Saturday Afternoon, Ballroom B
The leptin protein signal mediates homeostasis of energy intake, expenditure , storage, and reproduction. Leptin effects begin in utero, influencing future adaptive capacity as the fetus tailors its developmental trajectory to signals generated by maternal energy intake. Recent research associated variation in DNA methylation of the leptin gene (LEP) with timing of perinatal maternal nutritional insult and subsequent long-term health effects in humans, thus supporting the epigenetic hypothesis underlying fetal origins of disease. Yet, identification of variation in epigenetic architecture is incomplete. Leptin gene (LEP) expression is modulated by C/EBP α transcription factor binding site located in a core promoter CpG site. We compare methylation density of C/EBP αTFBS in three populations.
Our pilot study analyzed 50 maternal/offspring duos of migrant populations from West Africa, Ethiopia and Mexico. Mothers were born in their native countries, their offspring born in the United States. We pyrosequenced the LEP core promoter in DNA from peripheral blood. Mean levels of DNA methylation percentage in maternal samples are statistically different (Friedman's ANOVA: p = 0.007) for methylation of the C/EBP α TFBS site among populations: Ethiopians (62%), West Africans (36%) and Mexicans (43%). Offspring analysis is in progress to examine age and sex variation. We suggest this site as a candidate for nutritional studies when examining vulnerability to obesity and other chronic diseases upon exposure to rapid and dramatic changes faced during modern migration.
Funded by Research and Sponsored Programs Small Grant from Western Washington University.