Fetal circulating human resistin increases in diabetes during pregnancy and impairs placental mitochondrial biogenesis.
Shaoning JiangApril M TeagueJeanie B TryggestadTimothy J LyonsSteven D ChernausekPublished in: Molecular medicine (Cambridge, Mass.) (2020)
Resistin is increased in fetal circulation of infants exposed to the diabetic milieu, potentially reflecting a response of monocytes/macrophages to hyperglycemia and metabolic stresses associated with diabetes during pregnancy. Increased exposure to resistin may contribute to mitochondrial dysfunction and aberrant energy metabolism characteristic of offspring exposed to diabetes in utero.