Genetically identical mice either become obese or stay lean because of differences in how a specific set of genes is regulated.

J. Andrew Pospisilik at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg, Germany, and his colleagues studied mice with a mutation in the protein TRIM28, which has been linked to variation in body mass. The mice fell into two groups: those that grew obese and those of a normal weight, with the obese animals showing reduced expression of a network of genes involved in controlling weight.

The researchers then looked at data from obese and normal-weight children, as well as from 13 pairs of identical twins — in which one twin was obese and the other was lean — and found similar patterns of gene expression to the TRIM28 mutant mice. Differences in maternal diet, communities of microorganisms or other environmental factors could be triggering the switch to obesity in mice, the authors say.

Cell 164, 353–364 (2016)