Although in our study we did not evaluate the browning of WAT, increased UCP1 expression on BAT of the offspring of RYGB female rats may constitute a mechanism to attempt to control mitochondrial ROS production and the development of pathologies, since BS did not re-establish the expressions of CI and CIII, and our group has already showed49 that maternal RYGB in rats can negatively affect the growth and insulin secretion of offspring, resulting in insulin resistance and β-cell dysfunction in adult life. The gene discussed is UCP1; the disease is Insulin resistance.