IR, hyperinsulinemia, and related defects in post-receptor signaling pathways—such as serine phosphorylation of insulin receptor substrate-1 (IRS-1), AKT phosphorylation, and GLUT4 translocation—have been shown to disturb glucose metabolism and enhance androgen biosynthesis in ovarian theca and granulosa cells [145,146]. Here, AKT1 is linked to hyperinsulinism.