Nonalcoholic fatty liver disease (NAFLD) is leading chronic liver syndrome worldwide. Gut microbiota dysbiosis significantly contributes to the pathogenesis and severity of NAFLD. However, its role is complex and even unclear. Treatment of NAFLD through chemotherapeutic agents have been questioned because of their side effects on health. In this review, we highlighted and discussed the current understanding on the importance of gut microbiota, its dysbiosis and its effects on the gut-liver axis and gut mucosa. Further, we discussed key mechanisms involved in gut dysbiosis to provide an outline of its role in progression to NAFLD and liver cirrhosis. In addition, we also explored the potential role of probiotics as a treatment approach for the prevention and treatment of NAFLD. Based on the latest findings, it is evident that microbiota targeted interventions mostly the use of probiotics have shown promising effects and can possibly alleviate the gut microbiota dysbiosis, regulate the metabolic pathways which in turn inhibit the progression of NAFLD through the gut-liver axis. However, very limited studies in humans are available on this issue and suggest further research work to identify a specific core microbiome association with NAFLD and to discover its mechanism of pathogenesis, which will help to enhance the therapeutic potential of probiotics to NAFLD.

/pdf/understanding-the-effects-of-gut-microbiota-dysbiosis-on-3yc7eyrvfh.pdf

Understanding the Effects of Gut Microbiota Dysbiosis on Nonalcoholic Fatty Liver Disease and the Possible Probiotics Role: Recent Updates.

Impact of encapsulation of probiotics in oil-in-water high internal phase emulsions on their thermostability and gastrointestinal survival

Recently, Akkermansia muciniphila an anaerobic member of the gut microbiota, has been proposed as a next-generation probiotic. The aim of this study was evaluation of the effect of alive and pasteurized A. muciniphila on health status, intestinal integrity, immune response, lipid metabolism, and gut microbial composition in normal-diet fed mice as well as direct effects of the bacterium on Caco-2 cell line. A total of 30 mice were distributed into three different groups, control, alive, and pasteurized A. muciniphila-treated group. After acclimation, control and treatment groups were administrated with PBS and 109 CFU/200µL of bacterial suspension for 5 weeks, respectively. Besides, Caco-2 separately exposed to alive, pasteurized A. muciniphila and PBS for 24 h. The results showed that administration of A. muciniphila leads to reduction in body, liver, and white adipose weight. Histology data revealed both treatments had no adverse effects in colon, liver, and adipose tissues as well as induced better gut structure. Moreover, biochemical parameters and inflammatory biomarkers in plasma demonstrated that pasteurized A. muciniphila had more pronounce effect. Furthermore, alive A. muciniphia had better effects on the modulation of gene expression related to fatty acid synthesis, energy homeostasis, and immune response in the liver; meanwhile, these effects in the adipose was more in the pasteurized A. muciniphila administration. More importantly, the improvement of gut health by enhancing strengthen intestinal integrity and maintaining immune homeostasis was seen in both treatments; notably, pasteurized A. muciniphila had more effective. Similarly, treatment with the pasteurized form more effectively upregulated tight junction and regulated immune response-related genes in Caco-2 cell line. Both treatments triggered the improvement of microbiota communities, particularly the alive form. Therefore, both forms of A. muciniphila could modulate lipid and immune homeostasis, improved some gut microbiota, and promoted the overall health, while all these effects were dominantly observed in pasteurized form. In conclusion, pasteurized A. muciniphila can be considered as new medical supplement to maintain health state and prevent diseases in normal mice through different mechanisms.

Comparative effects of alive and pasteurized Akkermansia muciniphila on normal diet-fed mice.

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with type 2 diabetes mellitus (T2DM). Sesquiterpene glycosides from loquat leaf achieved beneficial effects on metabolic syndromes such as NAFLD and diabetes; however, their specific activity and underlying mechanism on T2DM-associated NAFLD have not yet been fully understood. In the present study, we found that sesquiterpene glycoside 3 (SG3), a novel sesquiterpene glycoside isolated from loquat leaf, was able to prevent insulin resistance (IR), oxidative stress, and inflammation. In db/db mice, SG3 administration (25 and 50 mg/kg/day) inhibited obesity, hyperglycemia, and the release of inflammatory cytokines. SG3 (5 and 10 μM) also significantly alleviated hepatic lipid accumulation, oxidative stress, and inflammatory response induced by high glucose combined with oleic acid in HepG2 cells. Western blotting analysis showed that these effects were related to repair the abnormal insulin signaling and inhibit the cytochrome P450 2E1 (CYP2E1) and NOD-like receptor family pyrin domain-containing 3 (NLRP3), both in vivo and in vitro. In addition, SG3 treatment could decrease the ratio of Firmicutes/Bacteroidetes and increase the relative abundance of Lachnospiraceae, Muribaculaceae, and Lactobacillaceae after a high-throughput pyrosequencing of 16S rRNA to observe the changes of related gut microbial composition in db/db mice. These findings proved that SG3 could protect against NAFLD in T2DM by improving IR, oxidative stress, inflammation through regulating insulin signaling and inhibiting CYP2E1/NLRP3 pathways, and remodeling the mouse gut microbiome. It is suggested that SG3 could be considered as a new functional additive for a healthy diet.

Novel Sesquiterpene Glycoside from Loquat Leaf Alleviates Type 2 Diabetes Mellitus Combined with Nonalcoholic Fatty Liver Disease by Improving Insulin Resistance, Oxidative Stress, Inflammation, and Gut Microbiota Composition.

Herein, we used a HFD/F to induce NAFLD in mice and intervened with CQPC06 to determine the preventive effect of CQPC06 on NAFLD and its potential regulatory mechanism. C57BL/6J mice were fed with LFD, HFD/F, HFD/F supplemented with CQPC06, and HFD/F supplemented with LDBS for 8 weeks to test the properties of the probiotic. Biochemical and molecular biology methods were used to determine the levels of related indexes in mouse serum, liver tissue, epididymal fat, small intestine tissue, and feces. The results showed that CQPC06 exhibited satisfactory probiotic properties, significantly inhibited mouse weight gain, and decreased the liver index and serum lipid levels, including ALT, AKP, AST, TC, TG, LDL-C, LPS, and HDL-C levels. The HOMA-IR index calculated based on the blood glucose levels and serum insulin levels showed that the HOMA-IR index of NAFLD mice treated with CQPC06 significantly decreased. From the molecular biology level, CQPC06 significantly increased the mRNA and protein expression of PPAR-α, CYP7A1, CPT1, and LPL in NAFLD mouse livers, and decreased the expression of PPAR-γ and C/EBP-α. Furthermore, CQPC06 enhanced the expression of ZO-1, occludin, and claudin-1 in the small intestine of NAFLD mice, and decreased the expression of CD36. CQPC06 decreased the level of Firmicutes and increased the levels of Bacteroides and Akkermansia in the feces of NAFLD mice, and the ratio of Firmicutes/Bacteroides was significantly decreased. CQPC06 is highly resistant in vitro and survived in the gastrointestinal tract and exerted its probiotic effect, altered the intestinal microecology of NAFLD mice, and played an important role in NAFLD prevention through the unique anatomical advantages of the gut-liver axis. There was a clear preventive effect with high concentrations of CQPC06 and it was stronger than that of l-carnitine.

Lactobacillus fermentum CQPC06 in naturally fermented pickles prevents non-alcoholic fatty liver disease by stabilizing the gut-liver axis in mice.

Both steatosis and inflammation are key pathological events in the progression of non-alcoholic fatty liver disease (NAFLD). Probiotics are beneficial for the prevention and treatment of NAFLD. Bifidobacterium animalis subsp. lactis V9 (V9) is a newly isolated strain with favorable probiotic properties. The study aims to evaluate the effects and mechanisms of V9 on the hepatic steatosis and inflammatory responses in a rat model of NAFLD induced by high-fat diets (HFD). Our results showed that administration of V9 significantly attenuated the HFD-induced increases in alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, resulting in alleviated hepatic steatosis. V9 supplementation reduced the accumulation of hepatic triglyceride and free fatty acid,while increasing the levels of glycogen. Serum levels of glucose were also decreased in HFD rats administrated with V9. Meanwhile, the transcription of SREBP-1c and FAS was reduced, and the hepatic expression of phosphorylated-AMPK and PPAR-α was restored after V9 administration. V9 suppressed the production of inflammatory cytokines (e.g. IL-6, IL-1β, and TNF-α) in HFD-fed rats. The anti-inflammatory effects of V9 was found to be associated with the inhibition of hepatic expression of TLR4, TLR9, NLRP3, and ASC mRNA. Furthermore, the activation of ERK, JNK, AKT and NF-κB were suppressed by V9 treatment. These results indicate that Bifidobacterium lactis V9 improves NAFLD by regulating de novo lipid synthesis and suppressing inflammation through AMPK and TLR-NF-κB pathways, respectively.

/pdf/probiotic-bifidobacterium-lactis-v9-attenuates-hepatic-5089z8ukf1.pdf

Probiotic Bifidobacterium lactis V9 attenuates hepatic steatosis and inflammation in rats with non-alcoholic fatty liver disease

The aim of this study was to evaluate the effects of a complex Bacillus subtilis additive on the fermentation quality and bacterial community during the ensiling process of whole-plant corn silage (WPCS). The pH values of WPCS treated with the B. subtilis inoculant decreased faster than those of the control without inoculant, and significantly higher contents of lactic acid (LA) and acetic acid (AA) were observed. After 45 days of ensiling, the LA contents reached 7.95% (w/w). In the treatment group, the neutral detergent fibre (NDF) and acid detergent fibre (ADF) contents decreased significantly compared to the control, and the degradation rates of the NDF and ADF were 26.52% and 27.34% after 45 days, respectively. The deoxynivalenol (DON) content in the treatment group decreased to 205.67 μg/kg, which was significantly lower than the content of 382.51 μg/kg in the control group. The results indicated the positive effect of the B. subtilis inoculant in improving WPCS fermentation, especially in terms of degrading linocellulose and removing DON. The analysis of the bacterial community indicated that the B. subtilis inoculant resulted in an increased abundance of Lactobacillus, which contributed to the enhancement of LA production. The increased abundance of Bacillus possibly played a role in the degradation of NDF and ADF and the reduction in DON. Therefore, the complex B. subtilis additive could be used for the production of high-quality WPCS.

/pdf/effect-of-bacillus-additives-on-fermentation-quality-and-iad3erdv.pdf

Effect of Bacillus Additives on Fermentation Quality and Bacterial Community during the Ensiling Process of Whole-Plant Corn Silage

Advanced glycation end products (AGEs) cause damage to pancreatic β-cells and trigger oxidative stress and inflammation, which promotes the development and progression of diabetes and its complications. Therefore, it is important to inhibit the formation of AGEs as part of the treatment of diabetes. Allicin is a natural antimicrobial agent with abundant pharmacological activities, and recent studies have reported its therapeutic effects in diabetes; however, the mechanism of these therapeutic effects is still unclear. Thus, the purpose of this study was to further investigate the association between allicin treatment of diabetes and AGEs. First, we established a streptozocin (STZ)-induced diabetic rat model and treated the rats with allicin for six weeks. We measured glycolipid metabolism, AGE levels, receptor of advanced glycation end products (RAGE) levels, oxidative stress, and other related indicators. The results showed that allicin improved blood glucose and body weight, reduced lipid accumulation, and inhibited AGE formation in rats. Treatment with allicin also inhibited RAGEs and thereby prevented AGE activity, which, in turn, alleviated oxidative stress and promoted insulin secretion. To further verify the effect of allicin on AGEs, we also performed in vitro nonenzymatic glycation simulation experiments. These results showed that allicin inhibited the production of AGEs by suppressing the production of AGEs intermediates. Thus, our research suggests that allicin may alleviate diabetes by inhibiting the formation of AGEs and reducing RAGE levels to relieve oxidative stress and promote insulin secretion.

/pdf/allicin-alleviates-diabetes-mellitus-by-inhibiting-the-jp3g9v0s.pdf

Allicin Alleviates Diabetes Mellitus by Inhibiting the Formation of Advanced Glycation End Products

Introduction Allicin is a wide spectrum prebiotic for human health, but whether it can attenuate blood in diabetes patients is rarely reported. In this study, we built a rat model and investigated the effect of allicin on diabetes mellitus type 2 (T2DM). We found that allicin could effectively reduce blood glucose levels, regulate intestinal microbiota, reduce lipid and body weight accumulation, and systemic inflammation in T2DM rats. Methods The rat model of type 2 diabetes was made by streptozotocin, and different doses of allicin were given orally by gavage. The intestinal contents of diabetes rats were sequenced and analyzed by 16S technology, and the clinical indicators of rats were detected for joint analysis. Results Allicin can improve the intestinal flora of type 2 diabetes rats, enrich beneficial metabolites, reduce blood glucose, improve blood lipids, reduce systemic inflammation, and improve type 2 diabetes. Discussion Intestinal microbiome analysis showed that allicin gavage significantly regulated the structure and main components of the intestinal microbiota in T2DM rats. Allicin increased the abundance of probiotic microbes, such as Lactobacillus, Clostridium and Akkermansia, while it reduced pathogenic microbes, such as Enterobacter, Erysipelatoclostridium and Colidextribacter. Allicin gavage increased the abundance of intestinal short-chain fatty acids, such as acetic acid and propionic acid. Correlation analysis showed that the increased gut microbes by allicin gavage were significantly associated with health physiological parameters but negatively related to serum inflammatory factors such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-a), and hypersensitive C-reactive protein (hs-CRP). In addition, our study also suggests that allicin may have prebiotic effects on chronic liver injury. This study shows that allicin can regulate various clinical symptoms of T2DM and is a potential therapeutic drug for T2DM.

Allicin modulates the intestinal microbiota to attenuate blood glucose and systemic inflammation in type 2 diabetic rats

The Polysaccharide Extracts from Astragalus Mongholicus Bunge Protects Mice from Acetaminophen-Induced Hepatotoxicity by Modulating the Nrf-2/ARE, JNK and Autophagy Pathways

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Yan Yan

Author Tools

Chat about Author