Skip to main content
. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Am J Obstet Gynecol. 2016 Mar 10;215(1 Suppl):S1–S46. doi: 10.1016/j.ajog.2016.03.001

Figure 10. Putative mechanism for the involvement of inflammation-mediated placental dysfunction in fetal programming.

Figure 10

The adverse inflammatory maternal environments of gestational diabetes (GDM), preeclampsia or obesity can generate increased oxidative/nitrative stress and cause mitochondrial dysfunction in the placenta in a sexually dimorphic manner. This disrupts placental function and in turn may lead to alterations in placental-mediated regulation of maternal metabolism and fetal growth and differentiation and hence result in fetal programming.