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It induces systemic metabolic disturbances primarily through dysregulated interactions among adipose tissue, liver, and skeletal muscle ( In the liver, IR presents as selective hepatic insulin resistance: insulins ability to suppress gluconeogenesis is diminished, resulting in fasting hyperglycemia, whereas its stimulatory effect on DNL remains intact or even enhanced ( In skeletal muscle, IR impairs glucose clearance due to defective GLUT4 translocation, which forces the liver to compensate by redirecting excess glucose into lipogenesis via ChREBP-dependent metabolic reprogrammingconstituting a glucose-to-lipid maladaptive feedback loop ( At the metabolic level, hyperglycemia robustly promotes DNL through the ChREBPFASN/ACC pathway

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