METABOLIC LIVER DYSFUNCTION AND ALTERED STEROID METABOLISM IN ENDOMETRIAL HYPERPLASIA
Keywords:
Endometrial hyperplasia; metabolic liver dysfunction; MASLD; insulin resistance; SHBG; estradiol; steroid metabolism; obesity.Abstract
Endometrial hyperplasia develops in the setting of prolonged disturbance of hormonal regulation, yet the conventional concept of unopposed estrogen exposure does not fully explain the clinical and metabolic heterogeneity of the disease. Obesity, insulin resistance, hyperinsulinemia, dyslipidemia and ovulatory dysfunction are frequent in affected women and are also closely linked to metabolic liver dysfunction. This narrative review examines clinical evidence connecting liver metabolic status, steroid metabolism and endometrial hyperplasia. A structured PubMed/MEDLINE search covered 2010–2026, with earlier seminal studies retained when they were essential for understanding hepatic SHBG regulation or local steroid metabolism. Thirty-one topic-specific publications were included in the qualitative synthesis, and the review was organized in accordance with SANRA principles. The most consistent clinical associations were observed for obesity and insulin resistance, whereas evidence for an independent role of dyslipidemia was less uniform. Direct studies of steatotic liver disease in histologically confirmed endometrial hyperplasia remain scarce. Metabolic studies, however, consistently associate hepatic fat accumulation and insulin resistance with lower sex hormone-binding globulin (SHBG), a change that may alter steroid bioavailability without a marked increase in total circulating hormone concentrations. Current evidence therefore supports metabolic liver dysfunction as a potential component of a broader metabolic-hormonal phenotype rather than an established independent cause of endometrial hyperplasia. Studies that assess anthropometric variables, HOMA-IR, lipid profile, liver-related markers, SHBG and steroid hormones within the same cohort, while accounting for age, ovulatory function and menopausal status, are required to define the contribution of the liver more precisely.
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