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Pathophysiological pathways contribute to low-grade inflammation in polycystic ovary syndrome (PCOS). Glucose-induced oxidative stress by production of inflammatory cytokines leads to insulin resistance. Cytokines via effects on theca cells eventually create hyperandrogenism. Macrophage derived mononuclear cells resulted in adipocytes hypertrophy and in turn by secretion of inflammatory cytokine create low-grade chronic inflammation
