Research Groups

Childhood diabetes


Coordinators of the group

  • Josep Jiménez-Chillarón

The hypothesis of the foetal origin of adult disorders postulates that an adverse intrauterine environment may affect the growth of the foetus by producing permanent changes of gene expression in key cells and/or tissues. Such changes would persist after birth and could contribute to the development of chronic and complex disorders typical of adults, such as type 2 diabetes or obesity. Our laboratory's goal is to understand the molecular mechanisms that associate nutrition during intrauterine development with the risk of acquiring chronic disorders as an adult, with special emphasis on diabetes and obesity.

In order to understand the underlying molecular mechanisms, in our group we have developed an experimental model of foetal malnutrition that recapitulates the metabolic phenotype described in humans: malnourished mice in the uterus show low weight at birth and develop obesity, intolerance to glucose, and diabetes as from the 4th month of life.


  1. To study the role of epigenetic mechanisms in the development of type 2 diabetes in an experimental model of intrauterine growth retardation.
  2. To study the role of the glucocorticoids in the foetal programming mechanism of diabetes and obesity in the adult.
  3. To study the role of intrauterine and postnatal subnutrition on memory and learning patterns in young and adult mice.