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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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OUT-EX) and for time variable (pre-intervention as reference category) were also performed