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Because GLP-2 acts through subepithelial myofibroblasts, which are the same cell population implicated in intestinal fibrogenesis, the risk-benefit profile of GLP-2 agonism may differ substantially between mucosal UC, inflammatory ileal CD, and stricturing or penetrating CD phenotypes, and this phenotypic stratification should be a required feature of future trial design

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Moreover, mitochondrial dysfunction can affect the function of the endogenous antioxidant system, reducing the cells ability to resist oxidative stress, thus forming a vicious cycle and accelerating muscle atrophy [34]