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During the development of nonalcoholic fatty liver disease (NAFLD), disorders of the carnitine pool are considered important drivers, in which the LCAC profile changes significantly with the progression of NAFLD and provides key clues for revealing the complex pathogenesis of NAFLD [209, 210]

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These cells may also provide an avenue for the systemic entry of commensal and pathogenic bacteria ultimately facilitating their dissemination throughout the human host (Niess et al