A key adaptation enabling the fetus to survive in a limited energy environment may be the
reprogramming of mitochondrial function, which can have deleterious effects. Critical
questions are whether mitochondrial dysfunction progressively declines after birth, and if so,
what mechanism might underlie this process. To address this, we developed a model of
intrauterine growth retardation (IUGR) in the rat that leads to diabetes in adulthood. Reactive
oxygen species (ROS) production and oxidative stress gradually increased in IUGR islets …