Endocrine Influences on Liver Health in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age, defined by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. Beyond reproductive dysfunction, PCOS is intimately linked with metabolic disturbances that predispose to hepatic steatosis and its complications. Insulin resistance, a hallmark of PCOS, accelerates hepatic de novo lipogenesis and triglyceride storage, while androgen excess alters adipocyte function and promotes ectopic lipid deposition in the liver. Dysregulation of other endocrine axes—including growth hormone, thyroid hormones and the hypothalamic–pituitary–adrenal axis—further modulates hepatic lipid flux, inflammatory signalling and fibrogenesis. Adipokines and cortisol dynamics interact with sex steroids to shape the fibroinflammatory cascade, driving progression from simple steatosis to steatohepatitis and fibrosis. Integrating these hormonal pathways is essential for accurate risk stratification and for the development of targeted interventions that address both insulin-dependent and non-insulin endocrine dysfunction in women with PCOS.

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Technical terms

Polycystic ovary syndrome (PCOS): A multifactorial endocrine disorder in women, characterised by androgen excess, ovulatory dysfunction and polycystic ovaries, with systemic metabolic consequences.

Non-alcoholic fatty liver disease (NAFLD/MASLD): A continuum of liver conditions defined by excessive hepatic fat accumulation unrelated to significant alcohol consumption, spanning benign steatosis to steatohepatitis and fibrosis.

Insulin resistance: A diminished physiological response of target tissues to circulating insulin, leading to compensatory hyperinsulinaemia and metabolic dysregulation.

Hyperandrogenism: Elevated serum levels of androgenic hormones in women, driving ovarian dysfunction, adipose tissue alterations and increased metabolic risk.

Steatosis: Intracellular accumulation of triglycerides within hepatocytes, representing the earliest histopathological manifestation of fatty liver disease.

Fibroinflammation: The combined processes of fibrosis and chronic inflammation within liver tissue, underpinning progression to advanced liver injury.

References

1. Endocrine aspects of metabolic dysfunction-associated steatotic liver disease (MASLD): Beyond insulin resistance. Journal of Hepatology (2023).
2. The hepato-ovarian axis: genetic evidence for a causal association between non-alcoholic fatty liver disease and polycystic ovary syndrome. BMC Medicine (2023).
3. Molecular signature of adipose tissue in patients with both Non-Alcoholic Fatty Liver Disease (NAFLD) and Polycystic Ovarian Syndrome (PCOS). Journal of Translational Medicine (2013).
4. Insulin resistance and hyperandrogenism drive steatosis and fibrosis risk in young females with PCOS. PLOS ONE (2017).