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By attaching an acetyl group to the sulfur atom of cysteine within the glutathione tripeptide, SAG resists enzymatic degradation in the gastrointestinal tract, crosses cell membranes intact, and is then hydrolyzed intracellularly by cytoplasmic thioesterases to release free, bioactive GSH directly inside cells

This process ultimately promotes FAO and increases hepatic lipid consumption [36]

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The evidence base for GLP-1 receptor agonists in post-bariatric weight regain continues to expand, though large randomized controlled trials remain limited compared to primary obesity treatment