Integrating untargeted OMICS markers that link maternal BMI to adiposity and cardiovascular development in early childhood (R-7250)

Both undernutrition and overnutrition in utero are associated with an increased risk of cardiometabolic diseases and premature death in later life. The biological mechanisms behind these associations are still unclear, and a greater mechanistic understanding is needed to guide prevention strategies. Recent evidence, mainly from animal studies, suggests that epigenetic mechanism are involved in the fetal origins of disease. Epigenetic mechanisms other than DNA methylation as well as other OMICS levels have received less attention. This study will investigate the molecular mechanisms linking maternal BMI to offspring adiposity and cardiovascular health in 3 European birth cohorts. Recent developments in untargeted OMICS analyses provide a great opportunity for the discovery of early biomarkers of exposure and disease risk. This will be the first study on this topic that will combine genome-wide information from multiple molecular levels (methylation, microRNAs, gene expression, and metabolites), enabling an integrated investigation of biological pathways. This will also be the first OMICS study examining the association between maternal adiposity and offspring cardiovascular health. I will use molecular and phenotype measurements up to the age of 4 years, which enables the identification of persistent molecular changes related to both the exposure and the disease risk. Studies using such a two-step approach are scarce and are needed to provide evidence for a causal link.

Keywords:cardiovascular development, OMICS markers

Disciplines:General biology, Plant biology