Dumesic et al. (2008) reported that insulin may be an important mediator of oocyte developmental competence via a ligand-receptor regulating system. The compensatory response to IR is hyperinsulinemia, and increased insulin could cause an increase in androgen. Excess insulin enhances androgen production in ovarian TCs under the stimulation of LH, resulting in follicular arrest and anovulation eventually (Silvestris et al., 2018). In addition, increased androgen could result in oocytes of lower quality after maturation (Cano et al., 1997). This evidence concerns the gene PLOD1 and hyperinsulinism.