Endocrine Disorders and Metabolic Dysfunction-Associated Steatotic Liver Disease: A Narrative Review

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the hepatic manifestation of systemic metabolic dysregulation, strongly linked to type 2 diabetes, cardiovascular diseases, liver-related complications, and different types of malignancies. Although MASLD is associated with obesity and insulin resistance, it is increasingly recognized that the liver engages in complex crosstalk with several endocrine pathways, including thyroid function, sex and steroid hormone regulation, and growth hormone signaling. The pathophysiology of MASLD is multifactorial and complex, as reflected by its clinical range-from simple steatosis to cirrhosis. MASLD now affects about one-quarter of the global population, with its prevalence rising due to sedentary lifestyles, chronic caloric excess, and endocrine disturbances contributing to disease progression. Given the escalating prevalence of MASLD and its frequent concurrence with various endocrinopathies, understanding this relationship is critical for refining diagnostic accuracy and optimizing therapeutic strategies. This review aims to synthesize contemporary insights into the complex interactions between MASLD and selected endocrine disorders, elucidate underlying pathophysiological mechanisms, and underscore novel treatment paradigms. As MASLD remains a significant clinical challenge worldwide, its intersection with endocrine dys

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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