Our research is focused on systems biology and integrated -omics approaches to investigate the missing heritability of type 2 diabetes and gestational diabetes.

Type 2 diabetes (T2D) has a strong heritable component and shows a preferential maternal transmission, however the >650 variants discovered through GWAS explain less than 20% of T2D heritability.  Our research is focused on investigating the missing heritability of type 2 diabetes through investigation of parent-of-origin effects (POE) on common variants and rare de novo and loss-of-function mutations, which could explain the maternal transmission and relate to developmental programming.

Periconceptional, fetal and neonatal period is crucial for organ development. Maternal exposures during the periconceptional period and pregnancy may increase offspring risk of diabetes in later life and may partially explain the preferential maternal transmission of T2D. For instance, maternal hyperglycemia and consequent gestational diabetes increases offspring risk of macrosomia, obesity and T2D. This period therefore provides a window-of-opportunity to prevent adverse consequences in mother and child.

We apply a systems genetics approach integrating  high-throughput -omics and machine learning in large family and population-based cohorts as well as tissues of interest to dissect such maternal and paternal effects and how they can affect risk of diabetes and its related comorbidities.