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GLP-1-based therapies and resmetirom operate through distinct and potentially complementary mechanisms: while resmetirom exerts direct hepatic effects by activating THR- to enhance mitochondrial function, reduce hepatic lipogenesis, and promote lipid oxidation specifically in hepatocytes, GLP-1 RAs and multi-agonists address the upstream metabolic drivers of MASLD including insulin resistance, obesity, and systemic inflammation

Glucose-6-phosphate dehydrogenase deficiency, the UDP-glucuronosyl transferase 1A1 gene, and neonatal hyperbilirubinemia

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There should be no visible powder or floaters