Here we provide evidence that human resistin is increased in fetal circulation of infants exposed to the diabetic milieu and impairs placental mitochondrial biogenesis signaling. Increased resistin is likely a response of monocytes/macrophages to hyperglycemia and metabolic stresses associated with diabetes during pregnancy. Thus, resistin acts as a circulating factor linking inflammation and energy metabolism during fetal life and it may contribute to impaired placental mitochondrial metabolism in maternal diabetes.