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RISS 인기검색어
- 검색키워드
- 저자 : Kazuyoshi Kon (검색결과 2 건)
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The Effect of Intestinal Flora Modification on Alcoholic Liver Injury in Obese KK-A<sup>y</sup> Mice
( Kazuyoshi Kon ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Alcoholic hepatitis occurs with background of chronic drinking for many years and a history of recent excessive alcohol consumption, carrying a poor short-term prognosis. Recently, the overlap of metabolic syndrome and alcoholic liver disease is increasing in industrialized countries; however, the treatment of alcoholic hepatitis has not been established. Here we investigated the effect of intestinal flora modification using rifaximin (RFX), non-absorbed antibiotic, on liver injury following ethanol (EtOH)-feeding plus binge in obese KK-A<sup>y</sup> mice. Methods: Female 8-week-old KK-A<sup>y</sup> mice were fed a liquid diet containing 5% EtOH or a pair-fed control diet for 10 days. Some mice were given RFX (0.1 g/L) during the feeding period. At day 11, mice were sacrificed. Some mice received a single gavage of EtOH (4g/kg BW) or isocaloric dextrin maltose as controls, and then be sacrificed 6 h later. Some mice were euthanized without EtOH binge for collecting of small intestinal contents. The net amount of intestinal microbiota was quantified using aerobic and anaerobic conventional culturing techniques, and qualitatively evaluation analyzed by 16S rRNA sequencing. Results: Livers from EtOH group showed severe steatohepatitis; which were ameliorated by RFX. The treatment with RFX significantly prevented increase of oxidative stress and inflammatory cytokines in mice given EtOH-feeding plus binge. Portal endotoxin was increased after EtOH-feeding plus binge, and RFX significantly prevented the increase. Overexpression of hepatic mRNA levels for cell differentiation (CD)-14 and tolllike receptor (TLR)-2 and -4 following EtOH-feeding plus binge was also significantly prevented by RFX. The net amount of small intestinal bacteria was significantly increased after chronic EtOH feeding as compared to controls; RFX had no effect on the net amount of viable bacterial cells increased by chronic EtOH feeding. In the profile of small intestinal microbiota in the order level, EtOH-feeding dramatically increased the relative abundance of the Erysipelotrichales. RFX drastically reversed the Erysipelotrichales and enriched the Bacteroidales. Conclusions: EtOH-induced intestinal microbial changes are one of the key events in the pathogenesis of alcoholic liver disease. Intestinal flora modification has a potential to prevent alcoholic liver injury comorbid with obese.
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Kenichi Ikejima,Kazuyoshi Kon,Shunhei Yamashina 대한간학회 2020 Clinical and Molecular Hepatology(대한간학회지) Vol.26 No.4
Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcoholrelated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gutderived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis.
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