Developmental origins of adult metabolic disease

The combined epidemiologic, clinical, and animal studies clearly demonstrate that the intrauterine environment influences growth and development of the fetus and the subsequent development of adult diseases. There are critical specific windows during development, often coincident with periods of rapid cell division, during which a stimulus or insult may have long-lasting consequences on tissue or organ function after birth. Birth weight is only one marker of an adverse fetal environment, and confining studies to this population only may lead to erroneous conclusions regarding etiology. Studies using animal models of uteroplacental insufficiency suggest that mitochondrial dysfunction and oxidative stress play an important role in the pathogenesis of the fetal origins of adult disease.