scholarly journals Intestinal Microbiota Protects against MCD Diet-Induced Steatohepatitis

2019 ◽  
Vol 20 (2) ◽  
pp. 308 ◽  
Author(s):  
Kai Schneider ◽  
Antje Mohs ◽  
Konrad Kilic ◽  
Lena Candels ◽  
Carsten Elfers ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Neutrophil Infiltration ◽  
Microbiota Composition ◽  
Alcoholic Fatty Liver ◽  
Commensal Microbiota ◽  
Intestinal Dysbiosis ◽  
Physiological Relevance

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in western countries, with a continuously rising incidence. Gut-liver communication and microbiota composition have been identified as critical drivers of the NAFLD progression. Hence, it has been shown that microbiota depletion can ameliorate high-fat diet or western-diet induced experimental Non-alcoholic steatohepatitis (NASH). However, its functional implications in the methionine-choline dietary model, remain incompletely understood. Here, we investigated the physiological relevance of gut microbiota in methionine-choline deficient (MCD) diet induced NASH. Experimental liver disease was induced by 8 weeks of MCD feeding in wild-type (WT) mice, either with or without commensal microbiota depletion, by continuous broad-spectrum antibiotic (AB) treatment. MCD diet induced steatohepatitis was accompanied by a reduced gut microbiota diversity, indicating intestinal dysbiosis. MCD treatment prompted macroscopic shortening of the intestine, as well as intestinal villi in histology. However, gut microbiota composition of MCD-treated mice, neither resembled human NASH, nor did it augment the intestinal barrier integrity or intestinal inflammation. In the MCD model, AB treatment resulted in increased steatohepatitis activity, compared to microbiota proficient control mice. This phenotype was driven by pronounced neutrophil infiltration, while AB treatment only slightly increased monocyte-derived macrophages (MoMF) abundance. Our data demonstrated the differential role of gut microbiota, during steatohepatitis development. In the context of MCD induced steatohepatitis, commensal microbiota was found to be hepatoprotective.

Sinapine reduces non-alcoholic fatty liver disease in mice by modulating the composition of the gut microbiota

2019 ◽  
Vol 10 (6) ◽  
pp. 3637-3649 ◽  
Author(s):  
Youdong Li ◽  
Jinwei Li ◽  
Qingfeng Su ◽  
Yuanfa Liu
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Chronic Inflammation ◽  
Fatty Liver Disease ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Intestinal Dysbiosis ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is associated with low-grade chronic inflammation and intestinal dysbiosis.

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 P841 Evaluation of gut microbiota composition in NAFLD with UC pancolitis in clinical remission: a pilot study

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S650-S651
Author(s):  
S Cocciolillo ◽  
G De Palma ◽  
T Chen ◽  
M P Ghali ◽  
M Deschenes ◽  
...  
Keyword(s):  
Liver Disease ◽  
Pilot Study ◽  
Gut Microbiota ◽  
Clinical Remission ◽  
Transient Elastography ◽  
Rrna Gene ◽  
Microbiota Composition ◽  
Cross Sectional ◽  
Alcoholic Fatty Liver ◽  
Gut Microbiota Composition

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is the main cause of liver disease in Western countries and is a frequently reported comorbidity in inflammatory bowel disease (IBD). A complex interaction among polygenic predisposition, IBD-specific risk factors, microbiome, multiple environmental and patients’ factors could explain the development of NAFLD in IBD. Gut dysbiosis is increasingly recognised as an important player in NAFLD, as well as in IBD pathogenesis. So far, no study has examined the gut microbiota composition in IBD patients with NAFLD. We aimed to characterise faecal microbiota according to NAFLD status in a pilot cohort of ulcerative colitis (UC) pancolitis in clinical remission. Methods This was a cross-sectional pilot study using transient elastography (TE) with controlled attenuation parameter (CAP) to diagnose NAFLD in UC pancolitis patients in clinical remission, defined as partial Mayo score ≤1. NAFLD was diagnosed non-invasively as CAP ≥248 dB/m. Exclusion criteria included: use of corticosteroids in the last year and antibiotics or probiotics/prebiotics in the last 2 months prior to inclusion; significant alcohol intake (AUDIT-C <5); hepatitis B or C infection. Stool samples were collected within 12 h from TE with CAP evaluation. Gut microbiota composition was analysed by 16S rRNA gene sequencing with Illumina technique. Statistical analysis by NAFLD status was performed using Fisher’s exact or Mann–Whitney’s test as appropriate. Results A total of 11 UC pancolitis patients in clinical remission were included (mean age 53 years, 36.4% male, time since IBD diagnosis 16 years). NAFLD was diagnosed in 7 cases (63.6%, mean CAP 291 dB/m). Patients with pancolitis and NAFLD had higher BMI (mean 31 vs. 22 kg/m2, p = 0.006) as well as waist circumference (mean 100 vs. 81 cm, p = 0.006) compared with those without NAFLD, but no other differences in demographic, clinical or pharmacological parameters were found between pancolitis with or without NAFLD. Patients with pancolitis and NAFLD clustered separately from those without NAFLD, when computing Bray Curtis dissimilarities (tested with Adonis, p = 0.006). In addition, patients with pancolitis and NAFLD presented with decreased bacterial richness (p = 0.017) but not diversity. This was accompanied by a significant increase of Bacteroides spp. relative abundance in faecal samples of patients with pancolitis and NAFLD (q = 0.017). Conclusion This pilot study demonstrates, for the first time, that, in UC pancolitis patients, NAFLD associates with altered gut microbiota composition. Further studies are needed to understand the exact role of gut microbiota in UC pancolitis with NAFLD and to evaluate the use of microbiota-directed approaches for the treatment of NAFLD in these patients.

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