An ambitious EC-funded research initiative on epigenetics advancing towards systems biology 140

Epidemiological evidence shows that sub-optimal nutrition during early development increases risk for chronic non-communicable diseases, including obesity, insulin resistance, type 2 diabetes or cardiovascular disease. In addition, developmental programming of disease risk may be inherited into the following generation offspring through non-genomic mechanisms.

Our laboratory is interested in understanding how environmental factors (nutrition) during early mammalian development influence phenotypic variance (disease risk; diabetes) on exposed individuals and their progeny. Epigenetic mechanisms may link early nutritional imbalances with permanent changes in gene expression that lead to adult disease risk. Likewise, epigenetic mechanisms may also mediate nutritionally-induced inheritance of such phenotypes if the epigenetic alterations occur in cells from the germ line.

We have previously developed a mouse model of transgenerational non-genomic inheritance of diabetes by neonatal malnutrition. We are currently investigating the potential role of DNA methylation and piRNAs in mediating disease risk and transgenerational effects.

People involved:

• Dr. Marta Ramón-Krauel,
• Thais Pentinat,
• Débora Martínez.