Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver condition globally, and growing evidence indicates that dietary protein quality significantly affects its metabolic and gastrointestinal (GI) manifestations. High intakes of total and animal-based proteins are linked to increased hepatic steatosis, inflammation, and fibrosis, while imbalanced amino acid profiles may disrupt lipid metabolism, insulin sensitivity, and hepatocellular homeostasis . Conversely, insufficient protein intake impairs mitochondrial oxidation and reduces hepatoprotective gut metabolites such as SCFAs and OCFAs, exacerbating NAFLD progression. Objective This review synthesizes current evidence on how dietary protein quality—defined by source, amino acid profile, and intake level—affects NAFLD development and GI function. It further evaluates microbiota-mediated mechanisms that connect protein metabolism with liver inflammation and steatosis .

A structured literature search was performed using PubMed and Google Scholar, including randomized controlled trials, cohort studies, mechanistic experiments, and meta-analyses examining associations between protein quality, NAFLD severity, and GI outcomes. Studies assessing gut microbiota composition, intestinal permeability, SCFA production, mitochondrial metabolism, and amino acid–driven pathways were included

• High total and animal-derived protein intake correlates with increased hepatic fat, greater histological activity, and higher risk of progression to NASH. • Amino acids such as methionine, phenylalanine, serine, glycine, arginine, and proline show strong associations with NAFLD histological severity and metabolic dysregulation . • Excess protein consumption causes dysbiotic microbiota shifts—including reduced Bacteroides—and promotes pro-inflammatory metabolites and intestinal permeability, contributing to hepatic inflammation . • Plant-derived proteins improve insulin sensitivity, decrease hepatic fat deposition, and enhance microbial diversity, potentially reducing fibrosis risk. • Protein insufficiency disrupts mitochondrial fatty acid oxidation and reduces gut-derived hepatoprotective metabolites, worsening susceptibility to steatosis.

Dietary protein quality plays a critical role in NAFLD pathogenesis through metabolic, inflammatory, and gut–liver axis mechanisms. Emphasizing plant-based proteins, optimizing amino acid profiles, and ensuring adequate intake may mitigate hepatic steatosis and support GI health. Further high-quality RCTs are needed to develop evidence-based recommendations for protein type, dose, and timing in NAFLD prevention and management.