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in parallel, invasive or therapy-resistant subpopulations switch on fatty-acid uptake and -oxidation, importing long-chain acyls via CD36/FATP transporters and routing them through CPT1-dependent oxidation to generate ATP and acetyl-CoA when glucose is scarce, a dependency that sustains metastatic seeding and can be blunted by pharmacological FAO blockers [112, 113]

Third, although existing studies consistently demonstrate beneficial effects on hepatic steatosis and inflammation, the lack of head-to-head mechanistic and biomarker-based comparisons restricts the ability to distinguish between different GLP-1RAs or combination therapies in terms of their molecular pathways, immunemetabolic regulatory efficiency, and predictive biomarkers of therapeutic response

physiological levels), or by its effects on hepatic IGF1