Fig. 7.

A schematic representation illustrating our working hypothesis regarding the regulation and activation of gravid uterine AR signaling pathways after combined exposure of hyperandrogenism and INS resistance. The signaling pathway depicted is based on the findings of the current study. There is evidence that cytosolic AR is translocated to and/or exists in the mitochondrion in several cell types and thus might exert effects downstream of the hyperandrogenism, thus leading to mitochondrial dysfunction. Further studies are required to determine whether PCOS-induced uterine cell defects are due to the mitochondrial AR actions during pregnancy