Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis

Liu, Li; Dong, Wenxiao; Wang, Sinan; Zhang, Yujie; Li, Tianyu; Xie, Runxiang; Wang, Bangmao; Cao, Hailong

doi:10.1039/c8fo01143e

Cited by 112 publications

(69 citation statements)

References 52 publications

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“…Clostridium species catabolize cholic acid to deoxycholic acid for their growth [152]. It is reported that, in mice, deoxycholic acid increases intestinal permeability through the reduction of goblet cell number, suppression of mucin production, induction of low-grade inflammation, and suppression of tight junction protein (ZO-1) expression [153]. In terms of dietary factors that reduce Escherichia , there are many reports of sulfated polysaccharides (Table 4).…”

Section: Association Of Dietary Factor-induced Reduction Of Blood mentioning

confidence: 99%

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Fuke¹,

Nagata

Suganuma³

et al. 2019

Nutrients

184

127

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Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer’s disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health.

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Section: Association Of Dietary Factor-induced Reduction Of Blood mentioning

confidence: 99%

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Fuke¹,

Nagata

Suganuma³

et al. 2019

Nutrients

184

127

View full text Add to dashboard Cite

show abstract

“…Interestingly, high-fat diet has also been associated with NLRP3 activation and increased tumor susceptibility [162,169]. High-fat diet leads to an increase in deoxycholic acid levels in the intestine, which, in turn, disrupts the cell monolayer integrity by decreasing the expression of the tight junction protein ZO-1 [170]. This disruption in the mucosal barrier leads to an increased tissue inflammation, mediated by NLRP3, and further polarization of M2 macrophages [162].…”

Section: Impact Of Nlrs On Cancermentioning

confidence: 99%

NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

et al. 2019

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Innate immunity comprises several inflammation-related modulatory pathways which receive signals from an array of membrane-bound and cytoplasmic pattern recognition receptors (PRRs). The NLRs (NACHT (NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from Podospora anserina) and TP1 (telomerase-associated protein) and Leucine-Rich Repeat (LRR) domain containing proteins) relate to a large family of cytosolic innate receptors, involved in detection of intracellular pathogens and endogenous byproducts of tissue injury. These receptors may recognize pathogen-associated molecular patterns (PAMPs) and/or danger-associated molecular patterns (DAMPs), activating host responses against pathogen infection and cellular stress. NLR-driven downstream signals trigger a number of signaling circuitries, which may either initiate the formation of inflammasomes and/or activate nuclear factor κB (NF-κB), stress kinases, interferon response factors (IRFs), inflammatory caspases and autophagy. Disruption of those signals may lead to a number of pro-inflammatory conditions, eventually promoting the onset of human malignancies. In this review, we describe the structures and functions of the most well-defined NLR proteins and highlight their association and biological impact on a diverse number of cancers.

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“…Oxidative stress level of the intestine was closely related to the integrity of histological morphology 22,37,38 . Ileal mucosal permeability was shown to be protected by Se‐enriched Agaricus bisporus mushroom by upregulating the mRNA expression of GPx in rats 7 .…”

Section: Resultsmentioning

confidence: 98%

Cardamine hupingshanensis aqueous extract improves intestinal redox status and gut microbiota in Se‐deficient rats

et al. 2020

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BACKGROUNDAs an essential trace element for mammalian species, selenium (Se) possesses powerful antioxidant properties and is a potential regulator of intestinal microbiota. However, effects of Cardamine hupingshanensis aqueous extract (CE), rich in Se, on balancing the intestinal redox status and regulating gut microbiota have been neglected.RESULTSAn Se‐deficient rat model was established by feeding a low‐Se diet (LD) for 5 weeks and CE was then supplemented to LD or normal‐Se‐diet (ND) rats. Antioxidant enzyme activities and short‐chain fatty acids (SCFA) concentration were increased by CE in both LD and ND rats. CE improved the intestinal morphology of LD rats impaired by deficient Se. Intestinal microbiota demonstrated various changes; for example, Butyrivibrio was increased in LD rats, while Bacteroides, Christensenellaceae, Clostridiaceae and Blautia were enhanced in ND rats.CONCLUSIONOur findings provide evidence that CE shows potential in improving intestinal redox status and regulating gut microbiota. © 2020 Society of Chemical Industry

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Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis

Abstract: Deoxycholic acid (DCA) induced intestinal low grade inflammation and disrupted the mucosal physical and functional barriers, aggravating intestinal tumorigenesis.

Cited by 112 publications

References 52 publications

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

Cardamine hupingshanensis aqueous extract improves intestinal redox status and gut microbiota in Se‐deficient rats

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