Probiotics and Liver Disease

Sharma, Vishal; Garg, Shashank; Aggarwal, Sourabh

doi:10.7812/tpp/12-144

Cited by 47 publications

(27 citation statements)

References 45 publications

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“…Such an association includes transfer of molecules associated with the gut microbiome to the liver and vice versa [48]. A growing body of evidence indicated that gut-liver axis malfunction (small intestinal bacterial overgrowth, intestinal dysbiosis, and increased intestinal permeability [“leaky gut”]) is a leading factor in the development and progression of NAFLD and obesity [49-53].…”

Section: Discussionmentioning

confidence: 99%

Paternal Programming of Liver Function and Lipid Profile Induced by a Paternal Pre-Conceptional Unhealthy Diet: Potential Association with Altered Gut Microbiome Composition

Zhang¹,

Dong²,

Sun³

et al. 2019

Kidney Blood Press Res

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Background/Aims: Paternal exposure to adverse environmental conditions can act on offspring’s phenotype and influence offspring’s later life disease risk. Our study was designed to examine the effect of feeding male rats before mating a high-fat, high-sucrose and high-salt diet (HFSSD) over two generations (F0 and F1) on their offspring’s (F2) liver function and gut microbiome composition. Methods: Male F0 rats and male F1 rats were fed either control diet or HFSSD before mating. Liver function of F2 offspring was investigated, and their gut microbiome composition was analyzed by 16S rRNA gene sequencing in the F2 offspring of rats whose fathers and grandfathers were fed with control diet (CD) (F0CD+F1CD-F2 group) or HFSSD prior to mating (F0HD+F1HD-F2 group). Results: F2 offspring had higher serum aspartate aminotransferase activity (female, p < 0.05 and male, p < 0.01 respectively) compared with control. Shannon indexes of gut microbiota indicated a significantly higher diversity in the female F0HD+F1HD-F2 as compared to F0CD+F1CD-F2 female offspring (p < 0.01). The dominant phyla of all the groups were Bacteroidetes, Firmicutes and Proteobacteria. There were significant differences in gut bacterial community composition at phyla and genus level between the F0CD+F1CD-F2 and F0HD+F1HD-F2. Furthermore, the variation in the relative abundance (percentage) of bacterial genus in the F2 offspring was associated with liver function alterations induced by a paternal pre-conceptional unhealthy diet. Male F0HD+F1HD-F2 offspring had higher serum cholesterol, high density lipoproteins as well as low density lipoproteins concentrations compared to the corresponding male control rats. Conclusion: Taken together, our findings suggested that a paternal pre-conceptional unhealthy diet predisposes the offspring to mild liver function alterations and alterations of gut microbiota in later life. Effects on lipids were sex-specific and only seen in male offspring.

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Section: Discussionmentioning

confidence: 99%

Paternal Programming of Liver Function and Lipid Profile Induced by a Paternal Pre-Conceptional Unhealthy Diet: Potential Association with Altered Gut Microbiome Composition

Zhang¹,

Dong²,

Sun³

et al. 2019

Kidney Blood Press Res

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show abstract

“…Recent studies have shown that the innate immune system interacts with the intestinal microbiota during the development of obesity and autoimmunity and promotes the progression of chronic liver disease. [59][60][61] For instance, the impact of the gut microbiota on NAFLD pathogenesis has been established recently. NAFLD is a complex metabolic disease associated with perturbations of multiple triggering factors, including the gut microbiota and diet.…”

Section: Gut Microbiota and Liver Diseasementioning

confidence: 99%

Impact of the gut microbiota, prebiotics, and probiotics on human health and disease

Lin

Chang²,

et al. 2014

Biomed J

109

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“…Disruption of this barrier provides the opportunity for previously excluded antigens and endotoxins to enter the enterocytes and systemic circulation. This situation has been described as a "leaky gut" and the resulting phenomenon as metabolic endotoxemia (Sharma, Garg, & Aggarwal, 2013). TLR4 expressed in Kupffer cells is activated by the lipopolysaccharide (LPS)-binding protein CD14 complex which initiates an inflammatory cascade that involves mitogen and stress activated protein kinases, p38, interferon regulatory factor 3, Jun-Nterminal kinase, and the nuclear factor kappa β (NF-κB) (Ruiz et al, 2007;Thuy et al, 2008).…”

Section: Roles Of the Microbiota In The Liver Immune Systemmentioning

confidence: 98%