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Microbes & Immunity Hydrogen alleviates non-alcoholic fatty liver disease

reduce the concentration of inflammatory factors in the to obesity and other diseases associated with metabolic
peripheral blood of patients with chronic obstructive abnormalities. Many studies have shown that A. muciniphila
pulmonary disease. A study by Yao et al. showed that regulates intestinal tight junction protein expression, and
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H -rich saline treatment ameliorated inflammation and reduced A. muciniphila abundance could increase intestinal
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apoptosis in myocardial ischemia/reperfusion through permeability, resulting in the leakage of harmful metabolites
PINK1/parkin-mediated mitochondrial autophagy. In from the gut into the blood and further to the liver along
recent years, our understanding of the association between the gut-liver axis; this leakage can damage the local
the gut microbiota and NAFLD has improved considerably, microenvironment and cause liver disease. Mice treated
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prompting the emergence of novel treatment approaches, with A. muciniphila also exhibited significantly reduced
including H administration. In this study, we confirmed serum TG and fasting blood glucose levels and increased
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the therapeutic effects of H on NAFLD, such as reversing insulin sensitivity. As the abundance of A. muciniphila
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the impairment of glucose tolerance; reducing the serum in the intestinal tract of HFD-fed mice decreases and the
concentrations of TG, TC, ALT, AST, LPS, and TNF-α; serum levels of LPS and TNF-α consequently increase.
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and alleviating hepatic steatosis. We clearly demonstrated Liver exposure to high concentrations of unwanted bacterial
that H therapy led to an increase in the relative abundance products, particularly LPS, also promotes the activation of
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of A. muciniphila in NAFLD model mice. Moreover, the inflammatory pathways and the release of circulating pro-
abundances of Faecalibacterium and Coriobacteriaceae_ inflammatory factors (such as TNF-α and IL-6), further
UCG-002 decreased significantly, and the FBR level contributing to liver tissue damage.
decreased following H treatment (Figure 4). Despite the interesting findings in the above, several
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Dysbiosis of the gut flora is known to impair intestinal limitations of this study should be acknowledged.
barrier function and associated immune responses. Ley Despite the encouraging hepatoprotective effect of H in
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et al. reported that FBR affects human susceptibility lowering the systematic pro-inflammatory factor levels,
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Figure 4. Effects of hydrogen (H ) intervention on non-alcoholic fatty liver disease (NAFLD) mice. This study confirmed the efficacy of H in the treatment
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of NAFLD. H alleviated the impairment of glucose tolerance; decreased the serum levels of triglyceride, total cholesterol, alanine aminotransferase,
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aspartate aminotransferase, lipopolysaccharide (LPS), and tumor necrosis factor-alpha (TNF-α); and alleviated hepatic steatosis. These results suggested
that H might improve intestinal permeability by increasing the abundance of Akkermansia muciniphila in the intestinal tract and subsequently reducing
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the amount of LPS produced by enteric pathogens, which produce TNF-α, in the liver through the portal vein. Thus, H has promising therapeutic
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potential for NAFLD based on the increasing abundance of A. muciniphila.
Volume 1 Issue 2 (2024) 77 doi: 10.36922/mi.3896