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Several studies have identified various sources of ROS and RNS in IBD, including neutrophils, macrophages, and inflamed intestinal tissue ( 2 Mechanism of oxidative stress in IBD While the precise mechanisms responsible for the development of IBD remain unclear, it is widely accepted that multiple factors contribute to its etiology, including overproduction of ROS, damage to biomolecules, mitochondrial dysfunction, recruitment of immune cells, impaired antioxidant defense system, and the activation of inflammatory pathways ( Figure 1 )
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Notably, because RYGB and VSG enhance the release of endogenous GLP-1 from enteroendocrine cells due to accelerated nutrient passage through the gut along with enhanced luminal bile acid signaling [10,11,12,13], this gut hormone was originally widely thought to contribute to their effects on food intake and body weight [14]
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