Nonalcoholic fatty liver disease (NAFLD) is widely emerging as the most prevalent
liver disorder and is associated with increased risk of liver-related and cardiovascular
mortality. Recent experimental and clinical studies have revealed the pivotal role
played by the alteration of gut-liver axis in the onset of fatty liver and related
metabolic disturbances. Gut-liver cross talk is implicated not only in the impairment
of lipid and glucose homeostasis leading to steatogenesis, but also in the initiation
of inflammation and fibrogenesis, which characterize nonalcoholic steatohepatitis
(NASH), the evolving form of NAFLD. The gut microbiota has been recognized as the
key player in the gut-liver liaison and because of its complexity can act as a villain or a victim. Gut microbiota not
only influences absorption and disposal of nutrients to the liver, but also conditions
hepatic inflammation by supplying toll-like receptor ligands, which can stimulate
liver cells to produce proinflammatory cytokines. Thus, the modification of intestinal
bacterial flora by specific probiotics has been proposed as a therapeutic approach
for the treatment of NASH. In this review, we summarized the evidence regarding the
role of gut-liver axis in the pathogenesis of NASH and discussed the potential therapeutic
role of gut microbiota modulation in the clinical setting.
Abbreviations:
ALT (alanine aminotransferase), BMP (bone morphogenetic protein), BT (bacterial translocation), CFU (colony-forming unit), DAMP (damage associated molecular patterns), FIAF (fasting-induced adipose factor), HSCs (hepatic stellate cells), IM (intestinal microbiota), IP (intestinal permeability), LPS (lipopolysaccharide), MetS (metabolic syndrome), NAFLD (nonalcoholic fatty liver disease), NASH (, nonalcoholic steatohepatitis), NF-kB (nuclear transcriptional factor kappa-B), PAMPs (pathogen-associated molecular patterns), RES (reticulumendothelial system), SIBO (small intestinal bacteria overgrowth), TGF-β (transforming growth factor β), TJ (tight junction), TLR (toll-like receptors), TNF-α (tumor necrosis factor alpha)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: August 11, 2015
Accepted:
August 4,
2015
Received in revised form:
August 1,
2015
Received:
March 18,
2015
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