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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
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& Matsumiya, G
Impairment of complex I leads to increased ROS production and decreased ATP synthesis, contributing to neuronal energy deficits and cell death [161]
Diabesity in the Arabian Gulf: challenges and opportunities
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