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A growing number of studies examining how dysbiosis might drive NAFLD have identified a number of plausible mechanisms, including changes in short-chain fatty acids (SCFAs) metabolism, increased intestinal permeability and lipopolysaccharides (LPS) activation of toll-like receptors (TLRs) and inflammasomes, endogenous ethanol production, decreased choline availability, and trimethylamine production (69)

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This mRNA distribution was echoed at the protein level, where the highest concentration of apical CFTR signal localized to cells with FOXI1 + nuclei, but a considerable amount of CFTR signal resided in other non-FOXI1 + cells (Fig