Endotoxins in Liver Disease

Nolan, James P.; Leibowitz, Alan I.

doi:10.1016/s0016-5085(19)31709-3

Cited by 22 publications

(14 citation statements)

References 3 publications

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“…84,85 Non-alcoholic fatty liver disease (NAFLD) is the most typical chronic liver complication observed in obesity and metabolic syndrome. This hepatic component of metabolic syndrome involves a complex expenditure.…”

Section: Gut Microbiota and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Cani

Osto²,

Geurts³

et al. 2012

Gut Microbes

762

512

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Obesity is associated with metabolic alterations related to glucose homeostasis and cardiovascular risk factors. These metabolic alterations are associated with low-grade inflammation that contributes to the onset of these diseases. We and others have provided evidence that gut microbiota participates in whole-body metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders. Recently, we defined gut microbiota-derived lipopolysaccharide (LPS) (and metabolic endotoxemia) as a factor involved in the onset and progression of inflammation and metabolic diseases. In this review, we discuss mechanisms involved in the development of metabolic endotoxemia such as the gut permeability. We also discuss our latest discoveries demonstrating a link between the gut microbiota, endocannabinoid system tone, leptin resistance, gut peptides (glucagon-like peptide-1 and -2), and metabolic features. Finally, we will introduce the role of the gut microbiota in specific dietary treatments (prebiotics and probiotics) and surgical interventions (gastric bypass).

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Section: Gut Microbiota and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Cani

Osto²,

Geurts³

et al. 2012

Gut Microbes

762

512

View full text Add to dashboard Cite

show abstract

“…Intestinal disruption can elevate portal endotoxemia by up to three-fold in healthy individuals on HFD [32], and 6 to 20-fold in individuals with NAFLD [33]. Portal endotoxemia can sensitize hepatic stellate cells and resident macrophages called Kupffer cells (KCs) to bacterial endotoxins including lipopolysaccharides (LPS), leading to liver fibrosis and cirrhosis (Figure 1) [34,35,36,37,38,39,40,41]. The potential mechanisms involved include endotoxin-mediated activation of toll-like receptor (TLR) 4 pro-inflammatory signaling [35,42], and the innate immune signaling complex called the inflammasomes (Figure 1) [43].…”

Section: Molecular Mechanisms Associated With Metabolic Syndrome mentioning

confidence: 99%

Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma: Implications for Lycopene Intervention

Wang

2013

Nutrients

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Increased prevalence of non-alcoholic fatty liver disease (NAFLD) is one of the consequences of the current obesity epidemic. NAFLD is a major form of chronic liver disease that is highly prevalent in obese and overweight adults and children. Nonalcoholic steatohepatitis (NASH) is the severe form of NAFLD, and uncontrolled inflammation as displayed in NASH has been identified as one of the key events in enhancing hepatic carcinogenesis. Lycopene is a non-provitamin A carotenoid and the pigment principally responsible for the characteristic deep-red color of ripe tomato and tomato products, as well as some fruits and vegetables. Lycopene’s innate antioxidant and anti-inflammatory properties have generated research interests on its capacity to protect against human diseases that are associated with oxidative stress and inflammation. In addition, differential mechanisms of lycopene metabolism including endogenous cleavage by carotenoid cleavage oxygenases (BCOs), generate lycopene metabolites that may also have significant impact on human disease development. However, it remains to be elucidated as to whether lycopene or its metabolites apolycopenoids have protective effects against obesity-related complications including inflammation and tumorigenesis. This article summarizes the in vivo experiments that elucidated molecular mechanisms associated with obesity-related hepatic inflammation and carcinogenesis. This review also provides an overview of lycopene metabolism, and the molecular pathways involved in the potential beneficial properties of lycopene and apolycopenoids. More research is clearly needed to fully unravel the importance of BCOs in tomato carotenoid metabolism and the consequence on human health and diseases.

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“…In addition, translocation of bacterial components termed pathogen-associated molecular patterns (PAMPs) triggers inflammatory responses through Toll-like receptors (TLRs) in both early and late disease stages (Dolganiuc et al, 2007; Fukui et al, 1991; Nolan and Leibowitz, 1978; Seki et al, 2007; Wiest and Garcia-Tsao, 2005). Moreover, PAMPs from the intestinal microbiota and TLR4 contribute to liver fibrosis and cirrhosis (Broitman et al, 1964; Rutenburg et al, 1957; Seki et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4

et al. 2012

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SUMMARY Increased translocation of intestinal bacteria is a hallmark of chronic liver disease and contributes to hepatic inflammation and fibrosis. Here we tested the hypothesis that the intestinal microbiota and Toll-like receptors (TLRs) promote hepatocellular carcinoma (HCC), a long-term consequence of chronic liver injury, inflammation and fibrosis. Hepatocarcinogenesis in chronically injured livers depended on the intestinal microbiota, and TLR4 activation in non-bone marrow-derived resident liver cells. TLR4 and the intestinal microbiota were not required for HCC initiation but for HCC promotion, mediating increased proliferation, expression of the hepatomitogen epiregulin, and prevention of apoptosis. Gut sterilization restricted to late stages of hepatocarcinogenesis reduced HCC suggesting that the intestinal microbiota and TLR4 represent therapeutic targets for HCC prevention in advanced liver disease.

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Endotoxins in Liver Disease

Cited by 22 publications

References 3 publications

Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma: Implications for Lycopene Intervention

Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4

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