Our previous studies demonstrate that maternal diabetes is associated with decreased PGC-1α/TFAM/mitochondrial biogenesis signaling in human placenta (Jiang et al. 2017). The present studies identify resistin as a potential mediator of that phenomenon by demonstrating increases in resistin concentration in the fetal circulation in pregnancies complicated by diabetes and inhibition of mitochondrial biogenesis and metabolism by resistin in the placenta. The production of resistin by fetal mononuclear cells reported here provides evidence for resistin as a link between the inflammatory response and energy metabolism in diabetes during pregnancy.