Gut-liver axis https://greenmedinfo.com/category/keywords/Gut-liver%20axis en Anti-inflammatory activities of green tea catechins along the gut-liver axis in nonalcoholic fatty liver disease. https://greenmedinfo.com/article/anti-inflammatory-activities-green-tea-catechins-along-gut-liver-axis-nonalcoh PMID:  J Nutr Biochem. 2020 Aug 12:108478. Epub 2020 Aug 12. PMID: 32801031 Abstract Title:  Anti-inflammatory Activities of Green Tea Catechins along the Gut-liver Axis in Nonalcoholic Fatty Liver Disease: Lessons Learned from Preclinical and Human Studies. Abstract:  Nonalcoholic fatty liver disease (NAFLD), which is the most prevalent hepatic disorder worldwide affecting 25% of the general population, describes a spectrum of progressive liver conditions ranging from relatively benign liver steatosis and advancing to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Hallmark features of NASH are fatty hepatocytes and inflammatory cell infiltrates in association with increased activation of hepatic nuclear factor kappa-B (NFκB) that exacerbates liver injury. Because no pharmacological treatments exist for NAFLD, emphasis has been placed on dietary approaches to manage NASH risk. Anti-inflammatory bioactivities of catechin-rich green tea extract (GTE) have been well-studied, especially in preclinical models that have detailed its effects on inflammatory responses downstream of NFκB activation. This review will therefore discuss the experimental evidence that has advanced an understanding of the mechanisms by which GTE, either directly through its catechins or potentially indirectly through microbiota-derived metabolites, limits NFκB activation and NASH-associated liver injury. Specifically, it will describe the hepatic-level benefits of GTE that attenuate intracellular redox distress and pro-inflammatory signaling from extracellular receptors that otherwise activate NFκB. In addition, it will discuss theanti-inflammatory activities of GTE on gut barrier function as well as prebiotic and antimicrobial effects on gut microbial ecology that help to limit the translocation of gut-derived endotoxins (e.g. lipopolysaccharides) to the liver where they otherwise upregulate NFκB activation by Toll-like receptor-4 signaling. This summary is therefore expected to advance research translation of the hepatic- and intestinal-level benefits of GTE and its catechins to help manage NAFLD-associated morbidity. <p><a href="https://greenmedinfo.com/article/anti-inflammatory-activities-green-tea-catechins-along-gut-liver-axis-nonalcoh" target="_blank">read more</a></p> https://greenmedinfo.com/article/anti-inflammatory-activities-green-tea-catechins-along-gut-liver-axis-nonalcoh#comments Catechin Green Tea Lipopolysaccharide-Induced Toxicity Nonalcoholic fatty liver disease (NAFLD) Anti-Inflammatory Agents NF-kappaB Inhibitor Gut-liver axis Review Tue, 25 Aug 2020 15:39:15 +0000 greenmedinfo 225788 at https://greenmedinfo.com Anti-obesity effects of Spirulina platensis protein hydrolysate by modulating brain-liver axis in high-fat diet fed mice https://greenmedinfo.com/article/anti-obesity-effects-spirulina-platensis-protein-hydrolysate-modulating-brain- PMID:  PLoS One. 2019 ;14(6):e0218543. Epub 2019 Jun 20. PMID: 31220177 Abstract Title:  Anti-obesity effects of Spirulina platensis protein hydrolysate by modulating brain-liver axis in high-fat diet fed mice. Abstract:  Spirulina platensis is a blue-green algae with potential anti-obesity effects. In this study, the anti-obesity effects of whole Spirulina platensis (WSP), Spirulina platensis protein (SPP) and Spirulina platensis protein hydrolysate (SPPH) were compared in high-fat diet fed mice, and the potential acting mechanism of SPPH was also investigated. Totally, SPPH exhibited good anti-obesity effects (reducing 39.8%±9.7% of body weight), lowering 23.8%±1.6% of serum glucose, decreasing 20.8%±1.4% of total cholesterol, while positive drug Simvastatin had the corresponding values: 8.3%±4.6%, 24.8%±1.9% and -2.1%±0.2%, respectively. Subsequently, PCR array was used to conduct gene expression analysis in brain and liver tissues of SPPH-treated mice, which displayed distinctly different expression pattern. The most markedly changed genes included: Acadm (-34.7 fold), Gcg (2.5 fold), Adra2b (2 fold) and Ghsr (2 fold) in brain; Retn (39 fold), Fabp4 (15.5 fold), Ppard (6 fold) and Slc27a1 (5.4 fold) in liver. Further network analysis demonstrated that the significantly expressed genes in brain and liver tissues were mapped into an interacting network, suggesting a modulatory effect on brain-liver axis, major pathways were involved in the axis: PPAR, adipocytokine, AMPK, non-alcoholic fatty liver disease and MAPK. This study showed that Spirulina platensis protein hydrolysate possessed anti-obesity effect in mice. <p><a href="https://greenmedinfo.com/article/anti-obesity-effects-spirulina-platensis-protein-hydrolysate-modulating-brain-" target="_blank">read more</a></p> https://greenmedinfo.com/article/anti-obesity-effects-spirulina-platensis-protein-hydrolysate-modulating-brain-#comments Obesity Spirulina Anti-Obesity Agents Gut-liver axis Animal Study Sat, 20 Jul 2019 02:02:48 +0000 greenmedinfo 191584 at https://greenmedinfo.com Arctic berry extracts target the gut-liver axis to alleviate metabolic endotoxaemia, insulin resistance and hepatic steatosis. https://greenmedinfo.com/article/arctic-berry-extracts-target-gut-liver-axis-alleviate-metabolic-endotoxaemia-i PMID:  Diabetologia. 2018 04 ;61(4):919-931. Epub 2017 Dec 21. PMID: 29270816 Abstract Title:  Arctic berry extracts target the gut-liver axis to alleviate metabolic endotoxaemia, insulin resistance and hepatic steatosis in diet-induced obese mice. Abstract:  AIMS/HYPOTHESIS: There is growing evidence that fruit polyphenols exert beneficial effects on the metabolic syndrome, but the underlying mechanisms remain poorly understood. In the present study, we aimed to analyse the effects of polyphenolic extracts from five types of Arctic berries in a model of diet-induced obesity.METHODS: Male C57BL/6 J mice were fed a high-fat/high-sucrose (HFHS) diet and orally treated with extracts of bog blueberry (BBE), cloudberry (CLE), crowberry (CRE), alpine bearberry (ABE), lingonberry (LGE) or vehicle (HFHS) for 8 weeks. An additional group of standard-chow-fed, vehicle-treated mice was included as areference control for diet-induced obesity. OGTTs and insulin tolerance tests were conducted, and both plasma insulin and C-peptide were assessed throughout the OGTT. Quantitative PCR, western blot analysis and ELISAs were used to assess enterohepatic immunometabolic features. Faecal DNA was extracted and 16S rRNA gene-based analysis was used to profile the gut microbiota.RESULTS: Treatment with CLE, ABE and LGE, but not with BBE or CRE, prevented both fasting hyperinsulinaemia (mean± SEM [pmol/l]: chow 67.2 ± 12.3, HFHS 153.9 ± 19.3, BBE 114.4 ± 14.3, CLE 82.5 ± 13.0, CRE 152.3 ± 24.4, ABE 90.6 ± 18.0, LGE 95.4 ± 10.5) and postprandial hyperinsulinaemia (mean ± SEM AUC [pmol/l × min]: chow 14.3 ± 1.4, HFHS 31.4 ± 3.1, BBE 27.2 ± 4.0, CLE 17.7 ± 2.2, CRE 32.6 ± 6.3, ABE 22.7 ± 18.0, LGE 23.9 ± 2.5). None of the berry extracts affected C-peptide levels or body weight gain. Levels of hepatic serine phosphorylated Akt were 1.6-, 1.5- and 1.2-fold higher with CLE, ABE and LGE treatment, respectively,and hepatic carcinoembryonic antigen-related cell adhesion molecule (CEACAM)-1 tyrosine phosphorylation was 0.6-, 0.7- and 0.9-fold increased in these mice vs vehicle-treated, HFHS-fed mice. These changes were associated with reduced liver triacylglycerol deposition, lower circulating endotoxins, alleviated hepatic and intestinal inflammation, and major gut microbial alterations (e.g. bloom of Akkermansia muciniphila, Turicibacter and Oscillibacter) in CLE-, ABE- and LGE-treated mice.CONCLUSIONS/INTERPRETATION: Our findings reveal novel mechanisms by which polyphenolic extracts from ABE, LGE and especially CLE target the gut-liver axis to protect diet-induced obese mice against metabolic endotoxaemia, insulin resistance and hepatic steatosis, which importantly improves hepatic insulin clearance. These results support the potential benefits of these Arctic berries and their integration into health programmes to help attenuate obesity-related chronic inflammation and metabolic disorders.DATA AVAILABILITY: All raw sequences have been deposited in the public European Nucleotide Archive server under accession number PRJEB19783 ( https://www.ebi.ac.uk/ena/data/view/PRJEB19783 ). <p><a href="https://greenmedinfo.com/article/arctic-berry-extracts-target-gut-liver-axis-alleviate-metabolic-endotoxaemia-i" target="_blank">read more</a></p> https://greenmedinfo.com/article/arctic-berry-extracts-target-gut-liver-axis-alleviate-metabolic-endotoxaemia-i#comments Berries: All Blueberry Cloudberry Crowberry Endotoxemia Hepatic Steatosis Insulin Resistance Lingonberry Obesity Hepatoprotective Gut-liver axis Plant Extracts Animal Study Tue, 12 Feb 2019 20:14:08 +0000 greenmedinfo 179556 at https://greenmedinfo.com Baicalin and the liver-gut system: Pharmacological bases explaining its therapeutic effects. https://greenmedinfo.com/article/baicalin-and-liver-gut-system-pharmacological-bases-explaining-its-therapeutic PMID:  Pharmacol Res. 2021 03 ;165:105444. Epub 2021 Jan 22. PMID: 33493657 Abstract Title:  Baicalin and the liver-gut system: Pharmacological bases explaining its therapeutic effects. Abstract:  With the development of high-throughput screening and bioinformatics technology, natural products with a range of pharmacological targets in multiple diseases have become important sources of new drug discovery. These compounds are derived from various plants, including the dried root of Scutellaria baicalensis Georgi, which is often used as a traditional Chinese herb named Huangqin, a popular medication used for thousands of years in China. Many studies have shown that baicalin, an extract from Scutellaria baicalensis Georgi, exerts various protective effects on liver and gut diseases. Baicalin plays a therapeutic role mainly by mediating downstream apoptosis and immune response pathways induced by upstream oxidative stress and inflammation. During oxidative stress regulation, PI3K/Akt/NRF2, Keap-1, NF-κB and HO-1 are key factors associated with the healing effects of baicalin on NAFLD/NASH, ulcerative colitis and cholestasis. In the inflammatory response, IL-6, IL-1β, TNF-α, MIP-2 and MIP-1α are involved in the alleviation of NAFLD/NASH, cholestasis and liver fibrosis by baicalin, as are TGF-β1/Smads, STAT3 and NF-κB. Regarding the apoptosis pathway, Bax, Bcl-2, Caspase-3 and Caspase-9 are key factors related to the suppression of hepatocellular carcinoma and attenuation of liver injury and colorectal cancer. In addition to immune regulation, PD-1/PDL-1 and TLR4-NF-κB are correlatedwith the alleviation of hepatocellular carcinoma, ulcerative colitis and colorectal cancer by baicalin. Moreover, baicalin regulates intestinal flora by promoting the production of SCFAs. Furthermore, BA is involved in the interactions of the liver-gut axis by regulating TGR5, FXR, bile acids and the microbiota. In general, a comprehensive analysis of this natural compound was conducted to determine the mechanism by which it regulates bile acid metabolism, the intestinal flora and related signaling pathways, providing new insights into the pharmacological effects of baicalin. The mechanism linking the liver and gut systems needs to be elucidated to draw attention to its great clinical importance. <p><a href="https://greenmedinfo.com/article/baicalin-and-liver-gut-system-pharmacological-bases-explaining-its-therapeutic" target="_blank">read more</a></p> https://greenmedinfo.com/article/baicalin-and-liver-gut-system-pharmacological-bases-explaining-its-therapeutic#comments Flavonoids Nonalcoholic fatty liver disease (NAFLD) Anti-Inflammatory Agents Gastrointestinal Agents NF-kappaB Inhibitor Gut-liver axis Animal Study Wed, 03 Nov 2021 17:32:48 +0000 greenmedinfo 248204 at https://greenmedinfo.com Bisphenol A exposure induces gut microbiota dysbiosis and consequent activation of gut-liver axis leading to hepatic steatosis. https://greenmedinfo.com/article/bisphenol-exposure-induces-gut-microbiota-dysbiosis-and-consequent-activation- PMID:  Environ Pollut. 2020 May 29 ;265(Pt A):114880. Epub 2020 May 29. PMID: 32540565 Abstract Title:  Bisphenol A exposure induces gut microbiota dysbiosis and consequent activation of gut-liver axis leading to hepatic steatosis in CD-1 mice. Abstract:  Interactions between the intestine and the liver, the so-called &#039;gut-liver axis&#039;, play a crucial role in the onset of hepatic steatosis and non-alcoholic fatty liver disease. However, not much is known about the impact of environmental pollutants on the gut-liver axis and consequent hepatic steatosis. Bisphenol A (BPA), a widely used plasticiser, is an important environmental contaminant that affects gut microbiota. We hypothesised that BPA induces hepatic steatosis by promoting gut microbiota dysbiosis and activating the gut-liver axis. In this study, male CD-1 mice were fed with diet containing BPA (50 μg/kg body weight/day) for 24 weeks. Dietary exposure to BPA increased lipid contents and fat accumulation in the liver. Analysis of 16 S rRNA gene sequencing revealed that the diversity of gut microbiota reduced and the composition of gut microbiota was altered in the BPA-fed mice. Further, theabundance of Proteobacteria, a marker of dysbacteria, increased, whereas the abundance of Akkermansia, a gut microbe associated with increased gut barrier function and reduced inflammation, markedly decreased. Expression levels of intestinal tight junction proteins (zona occludens-1 and occludin) also decreased drastically, leading to increased intestinal permeability and elevated levels of endotoxins. Furthermore, BPA up-regulated the expression of Toll-like receptor 4 (TLR4) and phosphorylation of nuclear factor-kappa B (NF-κB) in the liver and increased the production of inflammatory cytokines, including interleukin-1β, interleukin-18, tumour necrosis factor-α, and interleukin-6. Take together, our work indicated that dietary intake of BPA induced hepatic steatosis, and this was closely related to dysbiosis of gut microbiota, elevated endotoxin levels, and increased liver inflammation through the TLR4/NF-κB pathway. <p><a href="https://greenmedinfo.com/article/bisphenol-exposure-induces-gut-microbiota-dysbiosis-and-consequent-activation-" target="_blank">read more</a></p> https://greenmedinfo.com/article/bisphenol-exposure-induces-gut-microbiota-dysbiosis-and-consequent-activation-#comments Bisphenol Toxicity Dysbiosis Hepatic Steatosis Bisphenol A Gut-liver axis Animal Study Fri, 03 Jul 2020 20:15:49 +0000 greenmedinfo 223010 at https://greenmedinfo.com Bisphenol F exposure induces depression-like changes. https://greenmedinfo.com/article/bisphenol-f-exposure-induces-depression-changes PMID:  Environ Pollut. 2024 Jan 22 ;346:123356. Epub 2024 Jan 22. PMID: 38266696 Abstract Title:  Bisphenol F exposure induces depression-like changes: Roles of the kynurenine metabolic pathway along the &quot;liver-brain&quot; axis. Abstract:  Bisphenol F (BPF), one of the major alternatives of Bisphenol A (BPA), is becoming extensively used in industrial production with great harm to human beings and environment. Recent studies have revealed that environmental exposure is crucial to the initiation and development of depression. Thereby, the aim the present study is to ascertain the correlationship between the BPF exposure and depression occurrence. In the current study, BPF strikingly triggered depression-like changes in mice through the sucrose preference test (SPT), tail suspension test (TST) and forced swim test (FST), accompanied by the perturbation of the kynurenine (KYN) metabolic pathway along the &quot;liver-brain&quot; axis. Mechanistically, the neurotransmitters from the tryptophan metabolic pathway were converted to the toxic KYN pathway after BPF treatment. With the ELISA assay, it revealed that the toxic KYN metabolites, including KYN and 3-hydroxykynurenine (3-HK), were strikingly increased in the mouse brains which was ascribed to the enhanced expression of the rate-limiting enzymes Indoleamine 2,3-dioxygenase (IDO1) and Kynurenine 3-monooxygenase (KMO) respectively. Interestingly, the increased brain KYN induced by BPF was also validated partially from the periphery, since the ELISA and western blotting results indicated the significantly increased KYN in the serum and L-type amino acid transporter 1 (LAT1) in the brain, the key transporter responsible for KYN and 3-HK crossing the blood-brain barrier. Intriguingly, the liver-derived KYN metabolic pathway was the important source of the peripheral KYN and 3-HK, as BPF substantially enhanced hepatic IDO1, Tryptophan, 2, 3-dioxygenase (TDO2), and KMO levels indicated by western blotting. This study is the first to delineate previously unrecognized BPF-induced depression by regulating the KYN metabolic pathway along the &quot;liver-brain&quot; axis; therefore, targeting LAT1 or hepatic KYN signaling may provide a potentially unique therapeutic intervention in BPF-induced depression. <p><a href="https://greenmedinfo.com/article/bisphenol-f-exposure-induces-depression-changes" target="_blank">read more</a></p> https://greenmedinfo.com/article/bisphenol-f-exposure-induces-depression-changes#comments Bisphenol Toxicity Depression Bisphenol A Gut-liver axis Animal Study Thu, 14 Mar 2024 00:48:31 +0000 greenmedinfo 290418 at https://greenmedinfo.com Blueberry attenuated liver fibrosis, protected intestinal epithelial barrier, and maintained the homeostasis of the gut microbiota. https://greenmedinfo.com/article/blueberry-attenuated-liver-fibrosis-protected-intestinal-epithelial-barrier-an PMID:  Can J Gastroenterol Hepatol. 2019 ;2019:5236149. Epub 2019 Nov 22. PMID: 31886154 Abstract Title:  Blueberry Attenuates Liver Fibrosis, Protects Intestinal Epithelial Barrier, and Maintains Gut Microbiota Homeostasis. Abstract:  Objective: Recently, blueberry has been identified as a candidate for the treatment of liver fibrosis. Given the role of gut-liver axis in liver fibrosis and the importance of the gut microbiota homeostasis to the maintenance of the intestinal epithelial barrier, this study aimed to investigate whether blueberry could attenuate liver fibrosis and protect the intestinal epithelial barrier by maintaining the homeostasis of the gut microbiota.Method: A CCl-induced rat liver fibrosis model was used to detect the roles of blueberry in liver fibrosis and intestinal epithelial barrier. The liver weight and body weight were measured, the liver function was monitored by ALT and AST activity, protein and mRNA were determined by western blot and RT-qPCR, and the gut microbiome was detected by Miseq.Results: The results showed that blueberry could reduce the rate of liver weight/body weight gain (<p><a href="https://greenmedinfo.com/article/blueberry-attenuated-liver-fibrosis-protected-intestinal-epithelial-barrier-an" target="_blank">read more</a></p> https://greenmedinfo.com/article/blueberry-attenuated-liver-fibrosis-protected-intestinal-epithelial-barrier-an#comments Blueberry Liver Fibrosis Anti-Fibrotic Gastrointestinal Agents Gastroprotective Hepatoprotective Gut-liver axis Animal Study Thu, 30 Jan 2020 19:48:02 +0000 greenmedinfo 209973 at https://greenmedinfo.com Coffee prevents fatty liver disease induced by a high-fat diet by modulating pathways of the gut-liver axis. https://greenmedinfo.com/article/coffee-prevents-fatty-liver-disease-induced-high-fat-diet-modulating-pathways- PMID:  J Nutr Sci. 2019 ;8:e15. Epub 2019 Apr 22. PMID: 31037218 Abstract Title:  Coffee prevents fatty liver disease induced by a high-fat diet by modulating pathways of the gut-liver axis. Abstract:  Coffee consumption is inversely associated with the risk of non-alcoholic fatty liver disease (NAFLD). A gap in the literature still exists concerning the intestinal mechanisms that are involved in the protective effect of coffee consumption towards NAFLD. In this study, twenty-four C57BL/6J mice were divided into three groups each receiving a standard diet, a high-fat diet (HFD) or an HFD plus decaffeinated coffee (HFD+COFFEE) for 12 weeks. Coffee supplementation reduced HFD-induced liver macrovesicular steatosis ( <p><a href="https://greenmedinfo.com/article/coffee-prevents-fatty-liver-disease-induced-high-fat-diet-modulating-pathways-" target="_blank">read more</a></p> https://greenmedinfo.com/article/coffee-prevents-fatty-liver-disease-induced-high-fat-diet-modulating-pathways-#comments Coffee High Fat Diet Nonalcoholic fatty liver disease (NAFLD) Gastrointestinal Agents Hepatoprotective Gut-liver axis Animal Study Wed, 15 May 2019 18:47:35 +0000 greenmedinfo 187596 at https://greenmedinfo.com Continued alcohol misuse in human cirrhosis is associated with an impaired gut-liver axis. https://greenmedinfo.com/article/continued-alcohol-misuse-human-cirrhosis-associated-impaired-gut-liver-axis PMID:  Alcohol Clin Exp Res. 2017 Sep 19. Epub 2017 Sep 19. PMID: 28925102 Abstract Title:  Continued Alcohol Misuse in Human Cirrhosis is Associated with an Impaired Gut-Liver Axis. Abstract:  BACKGROUND: Cirrhosis and alcohol can independently affect the gut-liver axis with systemic inflammation. However, their concurrent impact in humans is unclear.METHODS: Our aim was to determine the effect of continued alcohol misuse on the gut-liver axis in cirrhotic patients. Age- and MELD-balanced cirrhotic patients who were currently drinking (Alc) or abstinent (NAlc) and healthy controls underwent serum and stool collection. A subset underwent upper endoscopy and colonoscopy for biopsies and duodenal fluid collection. The groups were compared regarding (i) inflammation/intestinal barrier: systemic tumor necrosis factor levels, intestinal inflammatory cytokine (duodenum, ileum, sigmoid), and ileal antimicrobial peptide expression; (ii) microbiota composition: 16SrRNA sequencing of duodenal, ileal, and colonic mucosal and fecal microbiota; and (iii) microbial functionality: duodenal fluid and fecal bile acid (BA) profile (conjugation and dehydroxylation status), intestinal BA transporter (ASBT, FXR, FGF-19, SHP) expression, and stool metabolomics using gas chromatography/mass spectrometry.RESULTS: Alc patients demonstrated a significant duodenal, ileal, and colonic mucosal and fecal dysbiosis, compared to NAlc and controls with lower autochthonous bacterial taxa. BA profile skewed toward a potentially toxic profile (higher secondary and glycine-conjugated BAs) in duodenal fluid and stool in Alc patients. Duodenal fluid demonstrated conjugated secondary BAs only in the Alc group. There was a greater expression of all ileal BA transporters in Alc patients. This group also showed higher endotoxemia, systemic and ileal inflammatory expression, and lower amino acid and bioenergetic-associated metabolites, without change in antimicrobial peptide expression.CONCLUSIONS: Despite cirrhosis, continued alcohol misuse predisposes patients to widespread dysbiosis with alterations in microbial functionality such as a toxic BA profile, which can lead to intestinal and systemic inflammation. <p><a href="https://greenmedinfo.com/article/continued-alcohol-misuse-human-cirrhosis-associated-impaired-gut-liver-axis" target="_blank">read more</a></p> https://greenmedinfo.com/article/continued-alcohol-misuse-human-cirrhosis-associated-impaired-gut-liver-axis#comments Alcohol Toxicity Cirrhosis: Liver Gut-liver axis Human Study Tue, 24 Oct 2017 02:36:38 +0000 greenmedinfo 154805 at https://greenmedinfo.com Diallyl disulfide ameliorates ethanol-induced liver steatosis and inflammation by maintaining the fatty acid catabolism and regulating the gut-liver axis. https://greenmedinfo.com/article/diallyl-disulfide-ameliorates-ethanol-induced-liver-steatosis-and-inflammation PMID:  Food Chem Toxicol. 2022 Jun ;164:113108. Epub 2022 May 5. PMID: 35526736 Abstract Title:  Diallyl disulfide ameliorates ethanol-induced liver steatosis and inflammation by maintaining the fatty acid catabolism and regulating the gut-liver axis. Abstract:  Diallyl disulfide (DADS) has been suggested to possess hepatoprotection against alcoholic liver disease (ALD) by a couple of pilot studies, while the underlying mechanisms remain largely unknown. This study aimed to investigate the hepatoprotective effects of DADS against ethanol-induced liver steatosis and early inflammation by using the chronic-plus-binge mice model and cultured J774A.1 macrophages and AML12 hepatocytes. We found that DADS significantly attenuated ethanol-induced elevation of serum aminotransferase activities, accumulation of liver triglyceride, hepatocytes apoptosis, oxidative stress, infiltration of macrophages and neutrophils, and proinflammatory polarization of macrophages in mice livers. In addition, chronic-plus-binge drinking induced apparent intestinal mucosa damage and disturbance of gut microbiota, endotoxemia, and activation of hepatic NF-κB signaling and NLRP3 inflammasome, which was inhibited by DADS. In vitro studies using cocultured AML12/J774A.1 cells showed that DADS suppressed ethanol/LPS-induced cell injury and inflammatory activation of macrophages. Furthermore, DADS ameliorated ethanol-induced decline of peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyltransferase 1 (CPT1), and phosphorylated AMP-activated protein kinase (AMPK) protein levels in mice livers and AML12 cells. These results demonstrate that DADS could prevent ethanol-induced liver steatosis and early inflammation by regulating the gut-liver axis and maintaining fatty acid catabolism. <p><a href="https://greenmedinfo.com/article/diallyl-disulfide-ameliorates-ethanol-induced-liver-steatosis-and-inflammation" target="_blank">read more</a></p> https://greenmedinfo.com/article/diallyl-disulfide-ameliorates-ethanol-induced-liver-steatosis-and-inflammation#comments Alcohol Toxicity Fatty Liver Inflammation Organosulfur Compounds Anti-Inflammatory Agents Hepatoprotective Gut-liver axis In Vitro Study Tue, 28 Jun 2022 23:45:27 +0000 greenmedinfo 259791 at https://greenmedinfo.com Dietary approach and gut microbiota modulation for chronic hepatic encephalopathy in cirrhosis. https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy- PMID:  World J Hepatol. 2019 Jun 27 ;11(6):489-512. PMID: 31293718 Abstract Title:  Dietary approach and gut microbiota modulation for chronic hepatic encephalopathy in cirrhosis. Abstract:  Hepatic encephalopathy (HE) is a common and serious neuropsychiatric complication of cirrhosis, acute liver failure, and porto-systemic shunting. HE largely contributes to the morbidity of patients with liver disease, severely affecting the quality of life of both patients and their relatives and being associated with poor prognosis. Its presentation is largely variable, manifesting with a broad spectrum of cognitive abnormalities ranging from subtle cognitive impairment to coma. The pathogenesis of HE is complex and has historically been linked with hyperammonemia. However, in the last years, it has become evident that the interplay of multiple actors, such as intestinal dysbiosis, gut hyperpermeability, and neuroinflammation, is of crucial importance in its genesis. Therefore, HE can be considered a result of a dysregulated gut-liver-brain axis function, where cognitive impairment can be reversed or prevented by the beneficial effects induced by&quot;gut-centric&quot;therapies, such as non-absorbable disaccharides, non-absorbable antibiotics, probiotics, prebiotics, and fecal microbiota transplantation. In this context dietary modifications, by modulating the intestinal milieu, can also provide significant benefit to cirrhotic patients with HE. This review will provide a comprehensive insight into the mechanisms responsible for gut-liver-brain axis dysregulation leading to HE in cirrhosis. Furthermore, it will explore the currently available therapies and the most promising future treatments for the management of patients with HE, with a special focus on the dietary approach. <p><a href="https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy-" target="_blank">read more</a></p> https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy-#comments Cirrhosis Encephalopathy Prebiotics Probiotics Gastrointestinal Agents Microbiota Transfer Therapy Gut-liver axis Microbiota Review Tue, 06 Aug 2019 18:52:06 +0000 greenmedinfo 192974 at https://greenmedinfo.com Effects of Pu-erh and Dian Hong tea polyphenols on the gut-liver axis. https://greenmedinfo.com/article/effects-pu-erh-and-dian-hong-tea-polyphenols-gut-liver-axis PMID:  AMB Express. 2023 Jun 2 ;13(1):53. Epub 2023 Jun 2. PMID: 37266757 Abstract Title:  Effects of Pu-erh and Dian Hong tea polyphenols on the gut-liver axis in mice. Abstract:  Tea polyphenols (TP) are the most biologically active components in tea, with antioxidant, antiobesity, and antitumor properties, as well as the ability to modulate the composition and function of intestinal microbiota. This experimental study evaluated the chemical constituents of polyphenols in Pu-erh (PTP) and Dian Hong tea (DHTP). It also investigated the co-regulatory effects of PTP and DHTP on intestinal flora and liver tissues in mice using 16 S rRNA gene and transcriptome sequencing. The results revealed that DHT had higher concentrations of EGC (epigallocatechin), C (catechin), EC (epicatechin), and EGCG (epigallocatechin gallate). In contrast, PT had higher concentrations of GA (gallic acid), ECG (epicatechin-3-gallate), TF (theaflavin), and TB (theabrownin). PTP and DHTP consumption significantly reduced the rates of weight gain in mice. Microbial community diversity was significantly higher in PTP and DHTP-treated mice than in the control group. Notably, beneficial microbes such as Lactobacillus increased significantly in PTP-treated mice, whereas Lachnospiraceae increased significantly in DHTP-treated mice. Both PTP and DHTP improved the activity of the antioxidant enzymes (SOD) and total antioxidant capacity (T-AOC) in the liver. The transcriptome analysis revealed that the beneficial effects of PTP and DHTP were due to changes in various metabolic pathways, the majority of which were related to antioxidant and lipid metabolism. This study discovered that PTP and DHTP had beneficial effects in mice via the gut-liver axis. <p><a href="https://greenmedinfo.com/article/effects-pu-erh-and-dian-hong-tea-polyphenols-gut-liver-axis" target="_blank">read more</a></p> https://greenmedinfo.com/article/effects-pu-erh-and-dian-hong-tea-polyphenols-gut-liver-axis#comments Black Tea Gastrointestinal Complaints Antioxidants Gut-liver axis Animal Study Sat, 19 Aug 2023 16:41:49 +0000 greenmedinfo 278539 at https://greenmedinfo.com Eugenol alleviated nonalcoholic fatty liver disease. https://greenmedinfo.com/article/eugenol-alleviated-nonalcoholic-fatty-liver-disease PMID:  Arch Biochem Biophys. 2022 May 1:109269. Epub 2022 May 1. PMID: 35508252 Abstract Title:  Eugenol alleviated nonalcoholic fatty liver disease in rat via a gut-brain-liver axis involving glucagon-like Peptide-1. Abstract:  Eugenol, an active ingredient of many medicinal aromatic plants, has been proved to have the hypolipidemic effect, but its potential mechanism of action is still unknown. This study aimed to investigate whether eugenol regulates liver lipid accumulation in high-fat diet (HFD) induced nonalcoholic fatty liver disease (NAFLD) rats via the gut-brain-liver axis involving glucagon-like peptide-1 (GLP-1). Hepatic vagotomy was performed in NAFLD rats to determine the role of eugenol in regulating hepatic lipid accumulation via vagus nerve. The results showed that after eight weeks of eugenol administration in NAFLD rats, serum total cholesterol (TC), triglyceride (TG) and hepatic TG decreased. However, eugenol showed no significant effect on the increased food intakes and weight gain caused by the HFD. Eugenol promoted the secretion of GLP-1 into the blood, increased GLP-1 receptor (GLP-1R) expression in the duodenum, liver, arcuate nucleus (ARC) and paraventricular nucleus (PVN), increased c-fos expression in the nucleus tractus solitarii (NTS), and promoted ZO-1 and occludin expression in duodenum. Furthermore, steatosis and lipid accumulation were significantly alleviated. Hepatic vagotomy partially attenuated the improvement of eugenol in hepatic lipid accumulation in NAFLD rats. In conclusion, eugenol regulates hepatic lipid metabolism via a gut-brain-liver axis involving in GLP-1, providing a new strategy for the treatment of NAFLD. <p><a href="https://greenmedinfo.com/article/eugenol-alleviated-nonalcoholic-fatty-liver-disease" target="_blank">read more</a></p> https://greenmedinfo.com/article/eugenol-alleviated-nonalcoholic-fatty-liver-disease#comments Eugenol Nonalcoholic fatty liver disease (NAFLD) Gastrointestinal Agents Hepatoprotective Hypolipidemic Gut-brain Axis Gut-liver axis Animal Study Sun, 08 May 2022 19:13:38 +0000 greenmedinfo 257387 at https://greenmedinfo.com Fermented ginseng improved alcohol liver injury in association with changes in the gut microbiota of mice. https://greenmedinfo.com/article/fermented-ginseng-improved-alcohol-liver-injury-association-changes-gut-microb PMID:  Food Funct. 2019 Sep 1 ;10(9):5566-5573. Epub 2019 Aug 20. PMID: 31429848 Abstract Title:  Fermented ginseng improved alcohol liver injury in association with changes in the gut microbiota of mice. Abstract:  The interactions among the liver, intestine and immune system play an important role in alcoholic liver injury. In this study, C57BL/6N mice with alcoholic injury were treated with unfermented and Lactobacillus fermentum KP-3-fermented ginseng. The indicators of hepatic steatosis, inflammation and injury were evaluated. The number of beneficial and harmful bacteria in the mice ileum and colon was counted by a traditional method; moreover, the diversity analysis of the cecum flora was performed. The alcohol exposure increased the levels of ALT, AST, TNF-α and IL-6 inflammatory factors and liver steatosis. In addition, the alcohol-fed miceexhibited a lower number of Lactobacilli and Bifidobacteria in the ileum and colon; the cecum flora diversity in the mice showed that alcohol obviously enhanced the abundance of the unclassified S24-7 of the Bacteroidetes phylum and the Proteobacteria genus of the Sutterella phylum and reduced the abundance of short-chain fatty acid-producing bacteria such as Akkermansia in the Verrucomicrobia phylum and those belonging to the Allobaculum genus, the Ruminococcus genus, and the Adlercreutzia genus in the Actinobacteria phylum. All these changes were improved by fermented ginseng. Conclusively, fermented ginseng could alleviate the alcoholic liver injury and disorder of the intestine by adjusting the intestinal flora. <p><a href="https://greenmedinfo.com/article/fermented-ginseng-improved-alcohol-liver-injury-association-changes-gut-microb" target="_blank">read more</a></p> https://greenmedinfo.com/article/fermented-ginseng-improved-alcohol-liver-injury-association-changes-gut-microb#comments Alcoholic Liver Disease Fermented Foods and Beverages Ginseng Gastrointestinal Agents Hepatoprotective Gut-liver axis Animal Study Mon, 13 Jan 2020 18:36:56 +0000 greenmedinfo 207939 at https://greenmedinfo.com Folic acid ameliorates alcohol-induced liver injury via gut-liver axis homeostasis. https://greenmedinfo.com/article/folic-acid-ameliorates-alcohol-induced-liver-injury-gut-liver-axis-homeostasis PMID:  Front Nutr. 2022 ;9:989311. Epub 2022 Oct 20. PMID: 36337656 Abstract Title:  Folic acid ameliorates alcohol-induced liver injurygut-liver axis homeostasis. Abstract:  The gut-liver axis (GLA) plays an important role in the development of alcohol-induced liver injury. Alcohol consumption is typically associated with folic acid deficiency. However, no clear evidence has confirmed the effect of folic acid supplementation on alcohol-induced liver injuryGLA homeostasis. In this study, male C57BL/6J mice were given 56% (v/v) ethanol and 5.0 mg/kg folic acid daily by gavage for 10 weeks to investigate potential protective mechanisms of folic acid in alcohol-induced liver injuryGLA homeostasis. Histopathological and biochemical analyses showed that folic acid improved lipid deposition and inflammation in the liver caused by alcohol consumption and decreased the level of ALT, AST, TG, and LPS in serum. Folic acid inhibited the expression of the TLR4 signaling pathway and its downstream inflammatory mediators in the liver and upregulated the expression of ZO-1, claudin 1, and occludin in the intestine. But compared with the CON group, folic acid did not completely eliminate alcohol-induced intestine and liver injury. Furthermore, folic acid regulated alcohol-induced alterations in gut microbiota. In alcohol-exposed mice, the relative abundance ofwas significantly increased, and the relative abundance ofwas significantly decreased. Folic acid supplementation significantly increased the relative abundance of,and, and decreased the relative abundance of. The results of Spearman&#039;s correlation analysis showed that serum parameters and hepatic inflammatory cytokines were significantly correlated with several bacteria, mainly including,, and. In conclusion, folic acid could ameliorate alcohol-induced liver injury in miceGLA homeostasis to some extent, providing a new idea and method for prevention of alcohol-induced liver injury. <p><a href="https://greenmedinfo.com/article/folic-acid-ameliorates-alcohol-induced-liver-injury-gut-liver-axis-homeostasis" target="_blank">read more</a></p> https://greenmedinfo.com/article/folic-acid-ameliorates-alcohol-induced-liver-injury-gut-liver-axis-homeostasis#comments Alcoholic Liver Disease Folic Acid Gastrointestinal Agents Hepatoprotective Gut-liver axis Animal Study Tue, 08 Nov 2022 18:59:18 +0000 greenmedinfo 266127 at https://greenmedinfo.com