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notably, the prevalence of IR remains significant even within the lean PCOS phenotype ( Driven by the IRhyperinsulinemiahyperandrogenism axis, metabolic imbalance directly disrupts follicular development, leading to chronic ovulatory dysfunction and deteriorating both oocyte quality and endometrial receptivity ( Insulin exerts a synergistic effect with gonadotropins on both granulosa and theca cells: hyperinsulinemia amplifies luteinizing hormone (LH) signaling and upregulates the expression of steroidogenic enzymes, thereby promoting ovarian and adrenal androgen synthesis