scholarly journals Role of Bile Acids and Gut Microbiota in Parenteral Nutrition Associated Injury

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Manithody Chandra Shekhara ◽  
Nispen Johan Van ◽  
Murali Vidul ◽  
Jain Sonali ◽  
Samaddar Ashish ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Parenteral Nutrition ◽  
Bile Acids ◽  
Associated Injury

scholarly journals Role of Bile Acids in Dysbiosis and Treatment of Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Caihua Wang ◽  
Chunpeng Zhu ◽  
Liming Shao ◽  
Jun Ye ◽  
Yimin Shen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Bile Acids ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Bile Acid Receptors

Nonalcoholic fatty liver disease (NAFLD) is a major health threat around the world and is characterized by dysbiosis. Primary bile acids are synthesized in the liver and converted into secondary bile acids by gut microbiota. Recent studies support the role of bile acids in modulating dysbiosis and NAFLD, while the mechanisms are not well elucidated. Dysbiosis may alter the size and the composition of the bile acid pool, resulting in reduced signaling of bile acid receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5). These receptors are essential in lipid and glucose metabolism, and impaired bile acid signaling may cause NAFLD. Bile acids also reciprocally regulate the gut microbiota directly via antibacterial activity and indirectly via FXR. Therefore, bile acid signaling is closely linked to dysbiosis and NAFLD. During the past decade, stimulation of bile acid receptors with their agonists has been extensively explored for the treatment of NAFLD in both animal models and clinical trials. Early evidence has suggested the potential of bile acid receptor agonists in NAFLD management, but their long-term safety and effectiveness need further clarification.

scholarly journals Role of Gut Microbiota in the Pathogenesis of Cardiovascular Diseases and Metabolic Syndrome

2018 ◽  
Vol 14 (4) ◽  
pp. 567-574 ◽  
Author(s):  
O. M. Drapkina ◽  
O. E. Shirobokikh
Keyword(s):  
Heart Failure ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Cardiovascular Diseases ◽  
Gut Microbiota ◽  
Bile Acids ◽  
G Protein ◽  
Short Chain Fatty Acids ◽  
Short Chain

The role of gut microbiota in the pathogenesis of cardiovascular diseases (CVD) and metabolic syndrome has attracted massive attention in the past decade. Accumulating evidence has revealed that the metabolic potential of gut microbiota can be identified as a contributing factor in the development of atherosclerosis, hypertension, heart failure, obesity, diabetes mellitus. The gut-host interaction occurs through many pathways including trimethylamine-N-oxide pathway (TMAO), short-chain fatty acids and second bile acids pathways. TMAO (the hepatic oxidation product of the microbial metabolite of trimethylamine) enhances platelet hyperreactivity and thrombosis risk and predicts major adverse cardiovascular events. Short-chain fatty acids and second bile acids, which are produced with the help of microbiota, can modulate host lipid metabolism as well as carbohydrate metabolism through several receptors such as G-protein-coupled receptors 41,43, farnesoid X-receptor, Takeda-G-protein-receptor-5. This way microbiota can impact host lipid levels, processes of weight gain, insulin sensitivity. Besides these metabolism-dependent pathways, there are some other pathways, which link microbiota and the pathogenesis of CVD. For example, lipopolysaccharide, the major component of the outer bacterial membrane, causes metabolic endotoxemia and low-grade systemic inflammation and contribute this way to obesity and progression of heart failure and atherosclerosis. This review aims to illustrate the complex interplay between microbiota, their metabolites, and the development and progression of CVD and metabolic syndrome. It is also discussed how modulating of gut microbiota composition and function through diet, prebiotics, probiotics and fecal microbiota transplantation can become a novel therapeutic and preventative target for CVD and metabolic syndrome. Many questions remain unresolved in this field and undoubtedly further studies are needed.

scholarly journals Chlorothalonil induces metabolic syndrome in mice by regulating host gut microbiota and bile acids metabolism via FXR pathways

2021 ◽  
Author(s):  
Zhiyuan Meng ◽  
Sen Yan ◽  
Wei Sun ◽  
Jin Yan ◽  
Miaomiao Teng ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Bile Acids ◽  
Low Dose ◽  
Daily Intake ◽  
Dependent Manner ◽  
Glycolipid Metabolism ◽  
Pesticides Exposure ◽  
Bile Acids Metabolism

Abstract Background：The most commonly used organochlorine pesticide, chlorothalonil (CHI), is ubiquitous in a natural environment and poses many adverse effects to organisms. Unfortunately, the toxicity mechanisms of CHI have not been clarified yet.Results: This study found that the low-dose CHI based on acceptable daily intake (ADI) level could induce metabolic syndrome (MetS) in mice, including obesity, hepatic steatosis, dyslipidemia, and insulin resistance. In addition, exposure to low-dose CHI could induce an imbalance in the gut microbiota of mice, resulting in a significant increase in the ratio of Firmicutes to Bacteroidetes. Furthermore, the results of the antibiotic treatment and gut microbiota transplantation experiments showed that the low-dose CHI could induce MetS in mice in a gut microbiota-dependent manner. Based on the results of targeted metabolomics and gene expression analysis, the low-dose CHI could disturb the serum metabolism of bile acids (BAs) in mice, causing the inhibition of the signal response of BAs receptor farnesol X receptor (FXR) and leading to glycolipid metabolism disorders in liver tissue and epididymal white adipose tissue (epiWAT) of mice. The administration of FXR agonist GW4064 and CDCA could significantly improve the low-dose CHI-induced MetS in mice.Conclusions: In conclusion, the low-dose CHI was found to induce MetS in mice by regulating the gut microbiota and BAs metabolism via the FXR signaling pathway. This study provides evidence linking the gut microbiota and pesticides exposure with the progression of MetS, demonstrating the key role of gut microbiota in the toxic effects of pesticides.

scholarly journals Parenteral Nutrition-Associated Liver Disease: The Role of the Gut Microbiota

Nutrients ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 987 ◽  
Author(s):  
Monika Cahova ◽  
Miriam Bratova ◽  
Petr Wohl
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Parenteral Nutrition

scholarly journals Role of the Gut–Liver Axis in Driving Parenteral Nutrition-Associated Injury

Children ◽  
2018 ◽  
Vol 5 (10) ◽  
pp. 136 ◽  
Author(s):  
Christine Denton ◽  
Amber Price ◽  
Julie Friend ◽  
Chandrashekhara Manithody ◽  
Keith Blomenkamp ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Parenteral Nutrition ◽  
Current Knowledge ◽  
Significant Risk ◽  
Associated Injury ◽  
Gut Function ◽  
Enteral Feedings ◽  
Cholestatic Liver Injury

For decades, parenteral nutrition (PN) has been a successful method for intravenous delivery of nutrition and remains an essential therapy for individuals with intolerance of enteral feedings or impaired gut function. Although the benefits of PN are evident, its use does not come without a significant risk of complications. For instance, parenteral nutrition-associated liver disease (PNALD)—a well-described cholestatic liver injury—and atrophic changes in the gut have both been described in patients receiving PN. Although several mechanisms for these changes have been postulated, data have revealed that the introduction of enteral nutrition may mitigate this injury. This observation has led to the hypothesis that gut-derived signals, originating in response to the presence of luminal contents, may contribute to a decrease in damage to the liver and gut. This review seeks to present the current knowledge regarding the modulation of what is known as the “gut–liver axis” and the gut-derived signals which play a role in PN-associated injury.

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