Mendelian randomization supports causality between maternal hyperglycemia and epigenetic regulation of leptin gene in newborns.

ABSTRACT: Leptin is an adipokine that acts in the central nervous system and regulates energy balance. Animal models and human observational studies have suggested that leptin surge in the perinatal period has a critical role in programming long-term risk of obesity. In utero exposure to maternal hyperglycemia has been associated with increased risk of obesity later in life. Epigenetic mechanisms are suspected to be involved in fetal programming of long term metabolic diseases. We investigated whether DNA methylation levels near LEP locus mediate the relation between maternal glycemia and neonatal leptin levels using the 2-step epigenetic Mendelian randomization approach. We used data and samples from up to 485 mother-child dyads from Gen3G, a large prospective population-based cohort. First, we bui

SUBMITTER: Allard C 

PROVIDER: S-EPMC4622547 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature