1 Evecare • Vol 11 • No. 2 • Sep–Dec 2023 Gynecologic Update Nonalcoholic Fatty Liver Disease inWomenWith Polycystic Ovary Syndrome: Understanding the Hepato–Ovarian Axis Research findings continue to hint at the correlation between polycystic ovary syndrome (PCOS) and hepatic diseases in women. PCOS, a disease characterized by hyperandrogenemia and ovarian dysfunction, is known to trigger nonalcoholic fatty liver disease (NAFLD).1 NAFLD, a condition with ≥ 5% fat accumulation in the liver, is considered the most common hepatic manifestation of PCOS. Several clinical studies reveal that NAFLD is more severe in women with PCOS, with higher rates of severe hepatocellular ballooning, fibrosis, and advanced fibrosis among them than that in those without PCOS.2 According to a few meta-analyses, women with PCOS have a 2-fold higher chance of developing NAFLD, independent of their BMI and the geographic region.2,3 The main risk factors for NAFLD in PCOS include hyperandrogenemia, insulin resistance (IR), obesity, chronic inf lammation, and genetic factors. As most women with NAFLD have IR, the association between NAFLD and IR has been widely accepted.2,3 This article discusses the role of PCOS-associated hyperandrogenemia in the manifestation of NAFLD. NAFLD Pathogenesis in a Hyperandrogenemic State A sustained increase in the gonadotropin-releasing hormone level in PCOS causes an increase in the secretion of luteinizing hormone (LH) and a decline in the secretion of follicle-stimulating hormone. An increased androgen effect on ovarian thecal cells because of the excessive LH activity leads to hyperandrogenemia, ovarian dysfunction, and metabolic disorders in women with PCOS.2 Hyperandrogenemia is an independent predictor of NAFLD in PCOS. The association between hyperandrogenemia and NAFLD risk in PCOS is supported by several biological mechanisms. Hyperandrogenemia can inf luence the development and progression of NAFLD in PCOS by affecting hepatic lipid metabolism and branchedchain amino acid metabolism and by causing inf lammation and an imbalance in apoptosis and autophagy.2 Impaired hepatic lipid metabolism In hyperandrogenic women with PCOS, excess androgens can suppress the transcription of the low-density lipoprotein receptor (LDLR) gene, thereby
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