Metabolic syndrome (MetS) represents a complex cluster of metabolic disturbances, including central obesity, insulin resistance, dyslipidemia, and arterial hypertension, which collectively contribute to systemic inflammation and endocrine dysfunction. In recent decades, increasing attention has been directed toward the influence of metabolic syndrome on female reproductive health, particularly ovarian structure and function. The ovaries are highly sensitive to metabolic and hormonal imbalance, and prolonged exposure to metabolic syndrome may induce profound pathological changes at the molecular, cellular, and tissue levels. These alterations manifest as disrupted folliculogenesis, stromal fibrosis, microvascular damage, chronic inflammation, oxidative stress, and hormonal dysregulation, often resulting in anovulation, infertility, and increased risk of polycystic ovary syndrome (PCOS).

This review summarizes current scientific evidence regarding the pathophysiological mechanisms linking metabolic syndrome to ovarian pathology. Special attention is paid to insulin resistance, hyperinsulinemia, adipokine imbalance, chronic low-grade inflammation, oxidative stress, and endothelial dysfunction as key mediators of ovarian structural damage. Morphological and histopathological changes observed in experimental models and clinical studies are discussed, including follicular atresia, theca cell hyperplasia, altered angiogenesis, and stromal remodeling. Understanding these mechanisms is essential for the development of targeted preventive and therapeutic strategies aimed at preserving ovarian function in women with metabolic syndrome.

metabolic syndrome, ovaries, insulin resistance, ovarian pathology, folliculogenesis, endocrine dysfunction

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