ReviewCurrent obesity reports2026
Hypothyroidism and Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanisms, Clinical Links, and Therapeutic Implications.
Review in Current obesity reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
purpose of reviewThis review evaluates the epidemiological, molecular, pathophysiological, and clinical relationships between hypothyroidism and metabolic dysfunction-associated steatotic liver disease (MASLD), with emphasis on hepatic lipid metabolism, mitochondrial function, insulin resistance, thyroid hormone signaling, and therapeutic implications. RECENT
findingsRecent observational studies and meta-analyses indicate a correlation between hypothyroidism, especially overt hypothyroidism, and a heightened risk of hepatic steatosis and fibrosis. Research indicates that thyroid-stimulating hormone might exert direct effects on the liver through signalling via thyroid-stimulating hormone receptors. Moreover, current research suggests that levothyroxine could enhance hepatic enzymes and steatosis in certain patients, whereas thyroid hormone receptor-β agonists have surfaced as potential liver-specific treatments for MASLD. The existing research indicates that thyroid dysfunction is a significant risk factor in MASLD. Regular evaluation of thyroid function might be suitable for certain patients with MASLD, and meticulous minimisation of metabolic risk is crucial. Nonetheless, the causal relationship is not fully determined, and additional longitudinal and mechanistic research is required to elucidate which patients would derive the greatest advantage from thyroid-targeted treatments.
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