Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rats

Sheng, Li; Wu, Weiping; He, Changyu; Zhou, Han; Jin, Dao-You; Wang, Lin

doi:10.3748/wjg.14.3254

Cited by 26 publications

(22 citation statements)

References 23 publications

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“…The authors also found an increased rate of small bowel overgrowth within these patients, as measured by glucose breath testing, suggesting that alterations in the microbiome may have contributed to disruption of gut barrier integrity. Similarly, studies of mouse models have found correlations between hepatic inflammation and measures of loss of intestinal barrier integrity, which further supports the hypothesis that loss of intestinal barrier integrity influences the pathogenesis of NAFLD and possibly NASH . Loss of this barrier function theoretically could expose the liver to increased levels of bacterial pro‐inflammatory products such as LPS, as well as toxic bacterial metabolic by‐products, including ethanol and other VOC such as ethanol, acetone and butanoic acid, among others.…”

Section: Resultssupporting

confidence: 56%

Systematic review: microbial dysbiosis and nonalcoholic fatty liver disease

Wieland

Frank

Harnke³

et al. 2015

Aliment Pharmacol Ther

177

143

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Summary Background The human intestinal microbiota is a key regulator of host metabolic and immune functions and alterations in the microbiome (‘dysbiosis’) have been implicated in several human diseases. Because of the anatomical links between the intestines and the liver, dysbiosis may also disrupt hepatic function and thereby contribute to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Aim To perform a comprehensive review of the medical literature investigating associations between intestinal dysbiosis and NAFLD, with a particular emphasis on studies that characterise the microbiome in NAFLD. Methods We conducted a search of PubMed, Embase, and Web of Science using multiple search terms including: ‘NAFLD, NASH, fatty liver, steatohepatitis’ combined with ‘metagenome, microbiom*, microbiota*, fecal flora, intestinal flora, gut bacteria’. Results were manually reviewed and studies selected based on relevance to intestinal microbiota and NAFLD. We also included studies that addressed potential mechanistic models of pathways linking the dysbiosis to NAFLD. Results Nine studies (five human and four animal models) were identified in our search that assessed associations between specific intestinal microbiota composition and NAFLD. We reviewed and summarised the results of additional investigations that more broadly addressed the mechanisms by which the microbiome may impact NAFLD pathogenesis. Conclusions Investigations in humans and animals demonstrate associations between intestinal dysbiosis and NAFLD; however, causality has not been proven and mechanistic links require further delineation. As the field of microbiome research matures in techniques and study design, more detailed insights into NAFLD pathogenesis and its associations with the intestinal microbiota will be elucidated.

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Section: Resultssupporting

confidence: 56%

Systematic review: microbial dysbiosis and nonalcoholic fatty liver disease

Wieland

Frank

Harnke³

et al. 2015

Aliment Pharmacol Ther

177

143

View full text Add to dashboard Cite

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“…An increase in intestinal permeability has been observed in some studies with NAFLD patients, but not in all (Table 1). However, an increased intestinal permeability in animal models and elevated endotoxin levels in both animals and NAFLD patients (34,37,(76)(77)(78)(79), further support the role of a decreased barrier function.…”

Section: Possible Contributing Factors and Mechanisms Of Intestinal Ementioning

confidence: 83%

Intestinal epithelial barrier function in liver cirrhosis: an extensive review of the literature

Pijls

Jonkers

Elamin

et al. 2013

Liver International

109

104

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Recent evidence suggests that translocation of bacteria and bacterial products, such as endotoxin from the intestinal lumen into the systemic circulation is a contributing factor in the pathogenesis of chronic liver diseases and the development of complications in cirrhosis. In addition to alterations in the intestinal microbiota and immune system, dysfunction of the intestinal epithelial barrier may be an important factor facilitating bacterial translocation. This review aims to provide an overview of the current evidence of intestinal epithelial barrier dysfunction in human chronic liver diseases and cirrhosis, and to discuss possible contributing factors and mechanisms. Data suggest the presence of intestinal epithelial barrier dysfunction in patients with chronic liver diseases, but are more convincing in patients with cirrhosis, especially in those with complications. The barrier dysfunction can result from both direct and indirect effects of aetiological factors, such as alcohol and obesity, which can cause chronic liver diseases and ultimately cirrhosis. On the other hand characteristics of cirrhosis itself, including portal hypertension, alterations in the intestinal microbiota, inflammation and oxidative stress can affect barrier function of both small and large intestine and may contribute to the development of complications. In conclusion, there are indications for intestinal epithelial barrier dysfunction in patients with chronic liver diseases and especially in patients with cirrhosis, which can be caused by various factors affecting both the small and large intestine.

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“…Occludin was regarded as one of the most important tight junction-associated structural proteins in the intestines and played a very important role in keeping physical barrier of intestinal mucosa49. Studies from Luca Miele et al .…”

Section: Discussionmentioning

confidence: 99%

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

Xue

Gao

et al. 2017

Sci Rep

236

165

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Gut-derived bacterial lipopolysaccharide (LPS) and subsequent hepatic toll-like receptor 4 (TLR4) activation have been recognized to be involved in the onset of diet-induced nonalcoholic fatty liver disease (NAFLD), but little is known about the variation of LPS and TLR4 during the progression of NAFLD. Probiotics were able to inhibit proliferation of harmful bacteria and improve gastrointestinal barrier function. However, it’s unclear whether LPS/TLR4 is involved in the protection effect of probiotics on NAFLD. In this study, we described characteristic of gut microbiota structure in the progression of NAFLD, and we also analyzed the relationship between gut microbiota and LPS/TLR4 in this process. Furthermore, we applied probiotics intervention to investigate the effect of probiotics on gut flora structure, intestinal integrity, serum LPS, liver TLR4 and liver pathology. Our results showed that serum LPS and liver TLR4 were highly increased during progression of NAFLD, with gut flora diversity and gut mircobiological colonization resistance (B/E) declining. Furthermore, probiotics could improve gut microbiota structure and liver pathology. Probiotics could also downregulate serum LPS and liver TLR4. Our results suggested that both gut flora alteration and endotoxemia may be involved in the progression of NAFLD. Probiotics may delay the progression of NAFLD via LPS/TLR4 signaling.

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Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rats

Cited by 26 publications

References 23 publications

Systematic review: microbial dysbiosis and nonalcoholic fatty liver disease

Systematic review: microbial dysbiosis and nonalcoholic fatty liver disease

Intestinal epithelial barrier function in liver cirrhosis: an extensive review of the literature

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

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