scholarly journals Amelioration of intestinal barrier dysfunction by berberine in the treatment of nonalcoholic fatty liver disease in rats

2017 ◽  
Vol 13 (52) ◽  
pp. 677 ◽  
Author(s):  
Donghao Li ◽  
Jimin Zheng ◽  
Yiting Hu ◽  
Hongtao Hou ◽  
Shurong Hao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Nonalcoholic Fatty Liver ◽  
Intestinal Barrier Dysfunction

scholarly journals Role of Gut Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xin Dai ◽  
Bangmao Wang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Barrier Function ◽  
Fatty Liver Disease ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Nonalcoholic Fatty Liver ◽  
Gut Barrier Function

Nonalcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease, and its incidence is increasing year by year. Many efforts have been made to investigate the pathogenesis of this disease. Since 1998 when Marshall proposed the conception of “gut-liver axis,” more and more researchers have paid close attention to the role of gut barrier function in the pathogenesis of NAFLD. The four aspects of gut barrier function, including physical, chemical, biological, and immunological barriers, are interrelated closely and related to NAFLD. In this paper, we present a summary of research findings on the relationship between gut barrier dysfunction and the development of NAFLD, aiming at illustrating the role of gut barrier function in the pathogenesis of this disease.

scholarly journals Translational Approaches with Antioxidant Phytochemicals against Alcohol-Mediated Oxidative Stress, Gut Dysbiosis, Intestinal Barrier Dysfunction and Fatty Liver Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 384
Author(s):  
Jacob W. Ballway ◽  
Byoung-Joon Song
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Leaky Gut ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Gut Dysbiosis ◽  
Disease States

Emerging data demonstrate the important roles of altered gut microbiomes (dysbiosis) in many disease states in the peripheral tissues and the central nervous system. Gut dysbiosis with decreased ratios of Bacteroidetes/Firmicutes and other changes are reported to be caused by many disease states and various environmental factors, such as ethanol (e.g., alcohol drinking), Western-style high-fat diets, high fructose, etc. It is also caused by genetic factors, including genetic polymorphisms and epigenetic changes in different individuals. Gut dysbiosis, impaired intestinal barrier function, and elevated serum endotoxin levels can be observed in human patients and/or experimental rodent models exposed to these factors or with certain disease states. However, gut dysbiosis and leaky gut can be normalized through lifestyle alterations such as increased consumption of healthy diets with various fruits and vegetables containing many different kinds of antioxidant phytochemicals. In this review, we describe the mechanisms of gut dysbiosis, leaky gut, endotoxemia, and fatty liver disease with a specific focus on the alcohol-associated pathways. We also mention translational approaches by discussing the benefits of many antioxidant phytochemicals and/or their metabolites against alcohol-mediated oxidative stress, gut dysbiosis, intestinal barrier dysfunction, and fatty liver disease.

scholarly journals Chitosan Oligosaccharide Ameliorates Nonalcoholic Fatty Liver Disease (NAFLD) in Diet-Induced Obese Mice

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 391 ◽  
Author(s):  
Minyi Qian ◽  
Qianqian Lyu ◽  
Yujie Liu ◽  
Haiyang Hu ◽  
Shilei Wang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Biological Effects ◽  
Intestinal Barrier ◽  
Integrated Analysis ◽  
Chitosan Oligosaccharide ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a global epidemic, and there is no standard and efficient therapy for it. Chitosan oligosaccharide (COS) is widely known to have various biological effects, and in this study we aimed to evaluate the liver-protective effect in diet-induced obese mice for an enzymatically digested product of COS called COS23 which is mainly composed of dimers and trimers. An integrated analysis of the lipidome and gut microbiome were performed to assess the effects of COS23 on lipids in plasma and the liver as well as on intestinal microbiota. Our results revealed that COS23 obviously attenuated hepatic steatosis and ameliorated liver injury in diet-induced obese mice. The hepatic toxic lipids—especially triglycerides (TGs) and free fatty acids (FFAs)—were decreased dramatically after COS23 treatment. COS23 regulated lipid-related pathways, especially inhibiting the expressions of FFA-synthesis-related genes and inflammation-related genes. Furthermore, COS23 could alter lipid profiles in plasma. More importantly, COS23 also decreased the abundance of Mucispirillum and increased the abundance of Coprococcus in gut microbiota and protected the intestinal barrier by up-regulating the expression of tight-junction-related genes. In conclusion, COS23, an enzymatically digested product of COS, might serve as a promising candidate in the clinical treatment of NAFLD.

scholarly journals The Role of Leaky Gut in Nonalcoholic Fatty Liver Disease: A Novel Therapeutic Target

2021 ◽  
Vol 22 (15) ◽  
pp. 8161
Author(s):  
Takaomi Kessoku ◽  
Takashi Kobayashi ◽  
Kosuke Tanaka ◽  
Atsushi Yamamoto ◽  
Kota Takahashi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Barrier Function ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Leaky Gut ◽  
Nonalcoholic Fatty Liver

The liver directly accepts blood from the gut and is, therefore, exposed to intestinal bacteria. Recent studies have demonstrated a relationship between gut bacteria and nonalcoholic fatty liver disease (NAFLD). Approximately 10%–20% of NAFLD patients develop nonalcoholic steatohepatitis (NASH), and endotoxins produced by Gram-negative bacilli may be involved in NAFLD pathogenesis. NAFLD hyperendotoxicemia has intestinal and hepatic factors. The intestinal factors include impaired intestinal barrier function (leaky gut syndrome) and dysbiosis due to increased abundance of ethanol-producing bacteria, which can change endogenous alcohol concentrations. The hepatic factors include hyperleptinemia, which is associated with an excessive response to endotoxins, leading to intrahepatic inflammation and fibrosis. Clinically, the relationship between gut bacteria and NAFLD has been targeted in some randomized controlled trials of probiotics and other agents, but the results have been inconsistent. A recent randomized, placebo-controlled study explored the utility of lubiprostone, a treatment for constipation, in restoring intestinal barrier function and improving the outcomes of NAFLD patients, marking a new phase in the development of novel therapies targeting the intestinal barrier. This review summarizes recent data from studies in animal models and randomized clinical trials on the role of the gut–liver axis in NAFLD pathogenesis and progression.

Role and Mechanisms of Probiotics in Regulating the ROS/JNK Signaling Pathway in the Pathogenesis of Nonalcoholic Fatty Liver Disease.

2021 ◽  
Author(s):  
HuiYuan Xu ◽  
LeiLei Yang ◽  
YuMei Huang ◽  
ChangPing Li
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Signaling Pathway ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Jnk Signaling ◽  
Nonalcoholic Fatty Liver ◽  
Jnk Signaling Pathway

Abstract This study was aimed to investigate the impact of probiotics on regulating the ROS/JNK signaling pathway their underlying mechanism of action in the treatment of nonalcoholic fatty liver disease. For this purpose, male C57BL/6 mice were randomly divided into three groups: control, probiotics, and model groups. Methionine and choline deficiency (MCD) diets were fed for four weeks to establish a NAFLD mouse model. Serum levels of ALT, AST, TC, and TG were detected. Moreover, the pathological changes of the liver and ileum tissues were observed by hematoxylin and eosin (H&E) staining, and the content of reactive oxygen species (ROS) in liver tissues was determined. In addition, the levels of D-lactic acid and plasma and small intestine diamine oxidase were measured to evaluate the effects of probiotics on the intestinal tract of NAFLD mice. The expression levels of p-JNK, Bax, and Caspase-3 were established to analyze the regulatory mechanism of probiotics on the JNK signaling pathway. We found that probiotics improve liver function, repair intestinal barrier and significantly suppressed oxidative stress, JNK phosphorylation. Moreover, the application of probiotics regulated the expression of signaling pathway-related proteins and promoted the intestinal barrier function repair and decreased intestinal permeability. The data above suggest that probiotics alleviate NAFLD, whose mechanism might be associated with the regulation of ROS/JNK signaling pathway and the suppression of oxidative stress and apoptosis.

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