Amelioration of non-alcoholic fatty liver disease by sodium butyrate is linked to the modulation of intestinal tight junctions in db/db mice

2020 ◽  
Vol 11 (12) ◽  
pp. 10675-10689
Author(s):  
Tingting Yang ◽  
Hao Yang ◽  
Cai Heng ◽  
Haiyan Wang ◽  
Shangxiu Chen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Protein Expression ◽  
Fatty Liver ◽  
Tight Junctions ◽  
Butyric Acid ◽  
Sodium Butyrate ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

T2DM–induced intestinal HG and intestinal barrier damage could co-inhibit GLP–1 secretion via suppressing intestinal TGR5 expression. Butyric acid secretes GLP–1 through the increase of TGR5 protein expression mediated by intestinal TJs and relieves inflammation.

scholarly journals The Intestinal Barrier and Its Dysfunction in Patients with Metabolic Diseases and Non-Alcoholic Fatty Liver Disease

2022 ◽  
Vol 23 (2) ◽  
pp. 662
Author(s):  
Roberta Forlano ◽  
Benjamin H. Mullish ◽  
Lauren A. Roberts ◽  
Mark R. Thursz ◽  
Pinelopi Manousou
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Metabolic Diseases ◽  
Intestinal Barrier ◽  
Gut Permeability ◽  
Alcoholic Fatty Liver ◽  
Treatment Pathways ◽  
New Treatment ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) represents an increasing cause of liver disease worldwide, mirroring the epidemics of obesity and metabolic syndrome. As there are still no licensed medications for treating the disease, there is an ongoing effort to elucidate the pathophysiology and to discover new treatment pathways. An increasing body of evidence has demonstrated a crosstalk between the gut and the liver, which plays a crucial role in the development and progression of liver disease. Among other intestinal factors, gut permeability represents an interesting factor at the interface of the gut–liver axis. In this narrative review, we summarise the evidence from human studies showing the association between increased gut permeability and NAFLD, as well as with type-2 diabetes and obesity. We also discuss the manipulation of the gut permeability as a potential therapeutical target in patients with NAFLD.

scholarly journals Hepatoprotective effects of Cassiae Semen on mice with non-alcoholic fatty liver disease based on gut microbiota

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Hanyan Luo ◽  
Hongwei Wu ◽  
Lixia Wang ◽  
Shuiming Xiao ◽  
Yaqi Lu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Therapeutic Effects ◽  
Alcoholic Fatty Liver ◽  
Hepatoprotective Effects ◽  
Underlying Mechanisms ◽  
Alcoholic Fatty Liver Disease

AbstractCassiae Semen (CS), the seeds of Cassia obtusifolia L. and C. tora L, have a long medicinal history in China, with suggestions for it to relieve constipation and exert hepatoprotective effects. However, the underlying mechanisms are still unclear. In this study, mice with high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) were used to study the hepatoprotective effects of CS. The relationship between gut microbiota and hepatoprotective effect mechanisms mediated by CS extracts, the total aglycone extracts of CS, rubrofusarin-6-β-gentiobioside, and aurantio-obtusin were examined. Our data indicate that CS extracts and components confer a protective effect by ameliorating lipid accumulation, intestinal barrier damage, liver damage, and inflammation on HFD-induced liver injury. Meanwhile, fecal microbe transplantation exerted the pharmacological effect of CS on HFD-fed mice; however, the efficacy of CS was inhibited or eliminated by antibiotic-induced dysbiosis. In conclusion, the therapeutic effects of CS on NAFLD were closely related to the gut microbiota, suggesting a role for TCM in treating disease.

scholarly journals Effect of tryptophan supplementation on diet-induced non-alcoholic fatty liver disease in mice

2014 ◽  
Vol 112 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Yvonne Ritze ◽  
Gyöngyi Bárdos ◽  
Astrid Hubert ◽  
Maureen Böhle ◽  
Stephan C. Bischoff
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Weight Ratio ◽  
Intestinal Barrier ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Junction Protein ◽  
Portal Plasma ◽  
Alcoholic Fatty Liver Disease

Intestinal serotonin (5-hydroxytrypamine, 5-HT) metabolism is thought to play a role in gut functions by regulating motility, permeability and other functions of the intestine. In the present study, we investigated the effect of tryptophan (TRP), the precursor of 5-HT, supplementation on intestinal barrier functions and non-alcoholic fatty liver disease (NAFLD). An established mouse model of NAFLD induced by feeding a fructose-rich diet (N group) was used in the present study. TRP was administered orally for 8 weeks to C57BL/6J control or NAFLD mice. NAFLD-related liver parameters (hepatic TAG and Oil Red O staining), intestinal barrier parameters (tight-junction protein occludin and portal plasma lipopolysaccharides (LPS)) and 5-HT-related parameters (5-HT, 5-HT transporter (SERT) and motility) were measured. We observed reduced duodenal occludin protein concentrations (P= 0·0007), high portal plasma LPS concentrations (P= 0·005) and an elevated liver weight:body weight ratio (P= 0·01) in the N group compared with the parameters in the control group. TRP supplementation led to an increase in occludin concentrations (P= 0·0009) and consecutively reduced liver weight:body weight ratio (P= 0·009) as well as overall hepatic fat accumulation in the N group (P= 0·05). In addition, the N group exhibited reduced SERT protein expression (P= 0·002), which was normalised by TRP supplementation (P= 0·02). For the first time, our data indicate that oral TRP supplementation attenuates experimental NAFLD in mice. The underlying mechanisms are not clear, but probably involve stabilisation of the intestinal barrier in the upper small intestine and amelioration of the dysregulated intestinal serotonergic system.

Gut Barrier Proteins Mediate Liver Regulation by the Effects of Serotonin on the Non-Alcoholic Fatty Liver Disease

2020 ◽  
Vol 21 (10) ◽  
pp. 978-984
Author(s):  
Ke Zhang ◽  
Xue Li ◽  
Xian Wang ◽  
Hongyu Zheng ◽  
Shusheng Tang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
The Body ◽  
Alcoholic Fatty Liver ◽  
High Fructose ◽  
Serotonin Reuptake Transporter ◽  
Liver Degeneration ◽  
Alcoholic Fatty Liver Disease

: Serotonin (5-hydroxytryptamine, 5-HT) has been recognized as a potent pro-inflammatory mediator. Increasing the bioavailability and preventing the formation of 5-HT can reduce the inflammatory response in the body. Moreover, 5-HT is considered as an important central physiologic mediator of intestinal function by regulating intestinal motility, permeability, and other functions. The dysfunction of intestinal serotonergic system causes intestinal barrier damage and further leads to the increase of bacterial endotoxin (LPS) translocation into the liver, which contributes to the development of non-alcoholic fatty liver disease (NAFLD). In addition, increasing the expression of serotonin reuptake transporter (SERT) and decreasing the expression of tryptophan hydroxylase1 (TPH1) can relieve the symptoms of NAFLD. Tryptophan (TRP), as a precursor of 5-HT synthesis, plays an important role in gut homeostasis and energy metabolism. Previous studies have found that TRP supplementation aggravates fatty liver degeneration by producing 5-HT, which activates mTOR signaling pathway in mice fed a high fat and high fructose diet. However, recent researches reveal that TRP supplementation stabilizes the intestinal barrier damage by increasing the expression of occludin and reduces the accumulation of fatty acids in liver. Although the effects of TRP supplementation on NAFLD are not clear and the specific mechanism needs to be further explored. A better understanding of the mechanisms of 5-HT on the liver and gut may open new therapeutic strategies in NAFLD.

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