In terms of lipid oxidative genes, including HMGCS2, CPT2 and CPT1A, no significant changes were observed (Figure 2C), indicating that lipid oxidation might not be responsible for the increased lipid deposition in liver, at least not in the early stages of hyperglycaemia or hyperlipidemia induced NAFLD. This evidence concerns the gene CPT1A and metabolic dysfunction-associated steatotic liver disease.