Intestinal permeability is increased in children with non-alcoholic fatty liver disease, and correlates with liver disease severity

Giorgio, Valentina; Miele, Luca; Principessa, Luigi; Ferretti, Francesca; Villa, Maria Pia; Negro, Valentina; Grieco, Antonio; Alisi, Anna; Nobili, Valério

doi:10.1016/j.dld.2014.02.010

Cited by 149 publications

(123 citation statements)

References 19 publications

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“…This process is dose-dependent and does not achieve saturation at up to 920 mg/dL of ethanol [11]. This is in line with the observations that (i) SIBO and gut hyperpermeability are closely associated with the progression from simple steatosis to NASH [6,[38][39][40][41][42], (ii) SIBO eradication with oral antibiotics prevents the development of both NAFLD and AFLD [43][44][45][46][47], (iii) germ-free mice are resistant to both diet-induced obesity and NAFLD [48,49], (iv) rats with experimentally-induced SIBO produce significantly more EE than controls, and (v) intragastric administration of sucrose in these animals elicits a 3-fold increase in portal concentrations of ACD with only modest elevation of systemic BAC [11].…”

Section: Discussionsupporting

confidence: 82%

Is nonalcoholic fatty liver disease an endogenous alcoholic fatty liver disease? – A mechanistic hypothesis

Medeiros

Lima

2015

Medical Hypotheses

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Section: Discussionsupporting

confidence: 82%

Is nonalcoholic fatty liver disease an endogenous alcoholic fatty liver disease? – A mechanistic hypothesis

Medeiros

Lima

2015

Medical Hypotheses

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“…NAFLD patients present increased gut permeability characterized by disruption of the intercellular TJs with decreased TJP ZO-1 expression, which is likely to allow translocations of bacteria and their products [44]. Intestinal permeability is increased in children with NAFLD, and correlates with the severity of steatohepatitis [45]. On the other hand, NASH patients were found to have endotoxemia and overexpression of TLR4 protein in the liver [46,47] associated with proinflammatory cytokine release and systemic inflammation.…”

Section: Nonalcoholic Fatty Liver Diseasesmentioning

confidence: 99%

Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation?

2016

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Background: Increased intestinal permeability due to barrier dysfunction is supposed to cause microbial translocation which may induce low-grade inflammation in various diseases. However, this series of events has not been comprehensively evaluated yet. Summary: Intestinal epithelial barrier dysfunction and increased permeability have been described in patients with inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), alcoholic liver disease, nonalcoholic steatohepatitis (NASH), liver cirrhosis, acute pancreatitis, primary biliary cholangitis (PBC), type 1 and type 2 diabetes, chronic kidney disease, chronic heart failure (CHF), depression, and other diseases. Most clinical reports used either permeability assays of challenge tests or measurement of circulating bacterial markers like endotoxin for assessment of ‘the leaky gut'. The intestinal permeability assessed by the challenge tests has often been related to the changes of tight junction proteins in the epithelium or circulating endotoxin levels. In patients with IBD, alcoholic liver disease, NASH, liver cirrhosis, PBC, obstructive jaundice, severe acute pancreatitis, and CHF, endotoxemia and proinflammatory cytokinemia have been found in addition to increased permeability. In the serum of patients with IBS and depression, antiflagellin antibodies and antilipid A antibodies were detected, respectively, together with increased permeability and proinflammatory cytokinemia. The site of infection, which is localized to the intestine in IBD and IBS, includes various extraintestinal organs in other diseases. The relation of gut dysbiosis to intestinal barrier dysfunction has gradually been clarified. Key Messages: Although no direct cause-and-effect relationship has been confirmed, all clinical and experimental data suggest the importance of intestinal hyperpermeability in the inflammatory changes of various diseases. Increased intestinal permeability is a new target for disease prevention and therapy. Considering the close relationship of ‘the leaky gut' and gut dysbiosis to the major diseases, we can conclude that meticulous dietetic and probiotic approaches to recover healthy microbiota have the potential to make a breakthrough in the management of these diseases tomorrow.

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“…One of the most important crosstalk between gut microbiota and humans is recognized as the above mentioned 'endotoxaemia' within NAFLD, characterized by elevated circulating lipopolysaccharide (LPS). In a recent study performed on NAFLD children, our research group shows that LPS blood level is increased in these patients, and that it is significantly higher in those with a more severe stage of liver disease [65]. Moreover, intravenous infusion of LPS in an acute human experimental study induces systemic insulin resistance and elevation of inflammatory markers in adipose tissue [66].…”

Section: Nalfd: the Liver At The Centermentioning

confidence: 89%

Nonalcoholic fatty liver disease as trigger of cardiovascular and metabolic complication in metabolic syndrome

et al. 2015

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Intestinal permeability is increased in children with non-alcoholic fatty liver disease, and correlates with liver disease severity

Cited by 149 publications

References 19 publications

Is nonalcoholic fatty liver disease an endogenous alcoholic fatty liver disease? – A mechanistic hypothesis

Is nonalcoholic fatty liver disease an endogenous alcoholic fatty liver disease? – A mechanistic hypothesis

Increased Intestinal Permeability and Decreased Barrier Function: Does It Really Influence the Risk of Inflammation?

Nonalcoholic fatty liver disease as trigger of cardiovascular and metabolic complication in metabolic syndrome

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