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These isogenic, mutation-specific cell lines have become a crucial tool for the pre-clinical screening and development of mutation-specific CFTR modulators (Valley et al., 2019)

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Collectively, these findings establish a mechanistic pathway whereby LEO restores dysregulated SCFA production in diabetic mice, highlighting dose-responsive butyrate accumulation as the dominant effector mediating enhanced GLP-1 secretion in functionally compromised enteroendocrine cells