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Experimental models, such as hepatocyte cultures treated with FFAs and insulin, have proven valuable for elucidating the pathophysiology and progression of NAFLD, as well as for testing potential therapeutic interventions [26] (Fig

Mechanistically, SFN led to dose-dependent upregulation of nuclear factor, erythroid 2 like 2 (Nrf2) and UDP glucuronosyltransferase 1A (UGT1A) expression

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Under such circumstances, up to 80% of the energy needs of the heart, skeletal muscle, and liver are derived from the oxidation of fatty acids in healthy individuals, whereas this transformation is compromised in those with fatty acid oxidation disorders (FAOD) [5, 6]