MASLD, diabetes and PMOS across the female life stages.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes, which affect approximately 38% and 10.5%, respectively, of adults globally, intersect critically in women through polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovary syndrome (PCOS), a prevalent but under-recognised cardiometabolic disorder affecting 10-13% of reproductive-age women. Beyond its reproductive consequences, PMOS promotes hepatic disease through hyperandrogenism, insulin resistance and chronic inflammation. Androgens directly upregulate hepatic lipogenic gene expression, activate hepatic stellate cells via androgen receptor signalling, and suppress sex hormone-binding globulin, creating a pro-fibrotic, lipotoxic hepatic environment. MASLD shares pathophysiological mechanisms with type 2 diabetes and PMOS, including adipose tissue dysfunction, adipokine dysregulation, hepatic lipid dysregulation and mitochondrial impairment. These shared mechanisms are further modulated by hormonal transitions during adolescence, pregnancy and menopause, with each representing a critical window of vulnerability. This narrative review consolidates current epidemiological and mechanistic insights linking MASLD, type 2 diabetes and PMOS in women, highlights the relevance of experimental models for elucidating shared disease pathways, and informs life stage-tailored screening and early intervention strategies to reduce long-term cardiometabolic and liver-related morbidity in affected women.