Liver health and gut health connection -
Doctors use liver function tests, liver ultrasound, CT scan or MRI scan to diagnose NAFLD, however some people will have to have biopsy.
The term gut—liver axis refers to the bidirectional relationship between the gut and the liver, which involves a complex relationship between the gut microbiome, the immune system, and the gut barrier. The liver communicates with the gut via a release of bile acids and antimicrobial molecules, such as immunoglobulins A IgA that help to regulate the gut microbiota and the immune system.
This process prevents the overgrowth of pathogenic microbes and keeps the gut barrier intact. The gut sends nutrients, microbiota byproducts that help to regulate liver glucose and lipid metabolism and recirculates bile acids back to the liver.
Dysbiosis and increased intestinal permeability leaky gut can lead to the movement of gut bacteria and into the portal vein supplying the liver.
As a result, an inflammation cascade is initiated in the liver as it becomes infiltrated by immune cells leading to liver injury. This in turn impairs the bile acid BA metabolism and promotes gut dysmotility and systemic inflammation. Evidence suggests that the stage of liver injury correlates closely with the severity of gut dysbiosis.
Some species-specific studies have identified particular bacteria called Akkermansia muciniphila with possible implications for obesity and NAFLD development. muciniphila is key increases the thickness of the mucus lining in the gut, hence optimising its barrier function.
muciniphila was found to correlate positively with a better metabolic health in mice and in human studies with obese and Type 2 Diabetes patients.
Interestingly, Helicobacter pylori has been identified to be present with a significant frequency in NAFLD patients, indicating a potential link between the presence of this bacteria and the development of fatty liver. There has also been a study suggesting certain mycobiome fungi composition can also contribute to NAFLD development.
Bacterial overgrowth in the gut and leaky gut have both been linked to the pathogenesis of NAFLD in humans. Large scale, longer-term research is warranted to establish if changes that occur in the bacteria and fungi compositions of the gut are causal or consequent of NAFLD development.
There is currently no standardized pharmacological treatment, and the only proven effective therapeutic strategy is lifestyle modification. Manipulation of the gut microbiome composition by probiotics and prebiotics show promise in NAFLD management.
Meta-analysis concluded that probiotic therapies can reduce liver enzymes, total-cholesterol, TNF-α and improve insulin resistance in NAFLD patients.
More robust randomised clinical trials are necessary to assess the clinical implications of probiotic and prebiotic therapy in NAFLD. Most commonly researched probiotic in NAFLD is VSL 3 — a mixture of probiotic bacteria including Lactobacilli that has been used in a number of experimental and human studies of NAFLD treatment and shown to improve liver enzymes and the severity of fat infiltration.
Omega-3 fatty acid treatment may also have a prebiotic effect in regulating liver lipid metabolism and inflammation.
Recent meta-analyses suggest that Omega3 fatty acids may be useful in the treatment of NAFLD and could have effects on the gut microbiota. It has been shown that Omega 3s increase Akkermansia and other beneficial bacteria.
Nutrition plays a pivotal role in the management of NAFLD. Studies show that NAFLD patients are more likely to consume high fat, energy-rich foods, saturated and omega-6 fatty acids and sweetened beverages, while not eating enough fresh fruits, green vegetables, fiber, and omega-3 fatty acids.
The Mediterranean diet is associated with a lower prevalence of NAFLD The Mediterranean Diet not only improves liver health on a clinical level, but there are improvements to inflammatory biomarkers, such as cytokines, involved in immune response.
Polyphenol rich foods such as cranberries, flaxseeds, grapes, black tea, fish oil which are part of the Mediterranean diet , increases the abundance of Akkermansia that keeps the gut lining healthy. These foods contain proanthocyanidins which have prebiotic activity. NAFLD is common and it may affect 1 in 5 people in the UK.
Since the lack of standardized pharmacological treatment to treat NAFLD, there is an increased interest in nutritional interventions for prevention and treatment of NAFLD. Research relieved the involvement of several components of the gut-liver axis such as microbiota dysbiosis, leaky gut, changes in bile acid metabolism, and reduction in SCFAs in progression of the NAFLD.
Gut and liver optimisation by Mediterranean dietary patterns rich in antioxidant rich plant foods and Omega 3s may offer an efficient approach to prevention and management of NAFLD. Although research is very promising, large trials are needed to establish the specific strains and dosages of probiotics in NAFLD.
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Tools My Gut Diary and Gut Health Assessments Booklet can help kickstart your gut health transformation Learn more. By The Gut Health Clinic team. What is NAFLD? What are the symptoms? People with more advanced NAFLD may suffer from: A dull or aching pain in the top right of the tummy over the lower right side of the ribs Extreme tiredness Unexplained weight loss Weakness How is it diagnosed?
Potential interventions Probiotics and Prebiotics There is currently no standardized pharmacological treatment, and the only proven effective therapeutic strategy is lifestyle modification. FXR receptor is also an inhibitor of BAs synthesis in the liver, which regulates BAs metabolism in enterohepatic circulation and can effectively control BAs content in the liver and intestine.
This provides feedback that if sufficient bile acids are absorbed in the ileum, new bile acids synthesis in the liver is inhibited. BAs regulates the ecosystem of gut microbiota and the interaction between the BAs and GM is a two-way direction Ridlon et al. Studies have shown that bile ducts blockages prevent bile from flowing into the intestines, which will cause the small intestinal bacterial overgrowth and translocation, and this could be reversed by BAs administration.
BAs binding to FXR could induce antimicrobial peptides AMPS production, which has a function in inhibiting the intestinal microbial overgrowth and intestinal barrier dysfunction Jiang et al.
Intestinal gut microbiota dysbiosis disrupts the balance between primary and secondary BAs Ridlon et al. The imbalance between BAs and intestinal bacteria leads to a series of host immune responses related to liver disease progression, bile acids regulate specific host metabolic pathways and modulate the inflammatory responses through FXR and G protein-coupled bile acid receptor 1 Marialena et al.
Gut microbes can also use bile acids to regulate the aggregation of NKT cells in mouse livers Ma et al. Choline, especially phosphatidylcholine, plays an important role in transporting lipids of the liver.
In the absence of choline, fat accumulates in the liver, which results in NAFLD. It is worth noting that rodents fed with a choline-deficient diet are often being used as models of non-alcoholic steatohepatitis NASH Valor et al.
Choline is not only important for liver function but also protects brain memory, enhances the brain to concentrate, improves motor ability, and delays the aging of the brain Derbyshire and Obeid, Choline can be converted to phosphatidylcholine lecithin by the host to assist the liver in excreting very-low-density lipoprotein VLDL particles Mehedint and Zeisel, This process prevents triglycerides accumulation in the liver.
However, gut microbiota such as Firmicutes and Proteobacteria can convert choline into trimethylamine TMA ; TMA can be transferred and converted to harmful metabolite trimethylamine N-oxide TMAO in the liver Coutinho-Wolino et al. The importance of methylamine is increasingly recognized, involving the liver, heart metabolism, and neurological disorders Chhibber-Goel et al.
Increased systemic circulation of TMAO is accompanied by a decreased level of phosphatidylcholine produced by the host Del Rio et al.
This imbalance is characteristic of intestinal disorders of patients. Free fatty acids include short-chain fatty acids SCFAs and long-chain fatty acids LCFAs.
SCFAs mainly include acetate, propionate, and butyrate, which are produced during the bacterial fermentation of dietary fibers Bergman, Butyrate could be used as the energy source of intestinal cells and helps to maintain the intestinal barrier functions Hamer et al.
Alcohol-induced liver injury is characterized by butyrate and propionate decreased, the level of acetate increased Peng et al.
Butyrate enhances the immune barrier of the intestinal mucosa, which prevents bacteria and their metabolites from entering the bloodstream and reducing the inflammatory response. Butyrate supplementation in glyceryl tributyl ester can reduce intestinal permeability disrupted by alcohol Cresci et al.
However, the mechanism through which tributyl glycerol protects the intestinal barrier remains unknown. LCFAs were also found closely connected with alcohol-induced liver injury. In the mice fed with an alcohol diet, the production of C and C was significantly decreased compared to the control fed with an isocaloric diet Shi et al.
In general, the level of total saturated LCFAs is positively correlated with the lumen abundance of Lactobacilli known metabolizers of saturated LCFAs. Saturated LCFA can promote colonic motility in rats and increase stool frequency Zhao et al.
Lactobacillus rhamnosus administration can increase the levels of luminal LCFA, and enhance its probiotic effects Shi et al. Alterations of gut microbiota compositions in different types of chronic liver diseases were summarized in Table 1.
Table 1 Alterations of gut microbiota compositions associated with Chronic Liver Disease. NAFLD is characterized by fat deposits in the liver and lipid metabolism disorders without significant alcohol consumption Angulo, NAFLD can develop into non-alcoholic steatohepatitis NASH , fibrosis, cirrhosis, and even hepatocellular carcinoma HCC Sun et al.
NAFLD has been considered as a multidirectional relationship with metabolic syndrome Godoy-Matos et al. According to GHE data in , NAFLD accounted for Lifestyles and dietary habits are closely related to the prevalence of NAFLD.
There is increasing evidence that NAFLD patients also have gut microbiota dysbiosis problems. A few microbiotas could be used as biomarkers to distinguish healthy individuals from patients with NAFLD, NASH, or cirrhosis Aron-Wisnewsky et al. Interestingly, it is the degree of cirrhosis, but not the NASH presence, which is related to intestinal leakage and intestinal bacterial overgrowth Miele et al.
The abundance of Bacteroides increased significantly and Firmicutes decreased in NASH groups when compared with the healthy control. Proteobacteria , Enterobacteriaceae , and Escherichia were significantly elevated in NASH. The possible mechanism of NASH is the intestinal alcohol-producing bacteria e.
Escherichia coli increased, more alcohol could provide a continuous source of ROS to the liver, leading to liver inflammation. Recently, the high-alcohol-producing Klebsiella Pneumoniae HiAlc Kpn was found in the gut of NASH patients. The NAFLD mouse model induced by HiAlc Kpn was also successfully established.
HiAlc Kpn with high ethanol production colonized the intestinal tract and produced a large amount of ethanol, which was transferred into the liver through the portal system, causing dysfunction of the liver Yuan et al.
It is reported that the mice deficient in junctional adhesion molecule A JAMA suffered more severe fatty liver and steatohepatitis than control mice when treated mice with a high saturated fat diet.
Antibiotics or sevelamer hydrochloride treatment can reduce the severity of fatty liver and steatohepatitis in JAMA deficient mice Rahman et al. Alcohol-related liver disease ALD accounts for 0. Drinking alcohol can increase the imbalance of intestinal bacteria and fungi, leading to the development of disease susceptibility, intestinal barrier function loss, and liver injury Bajaj, Cho et al.
reported that in ethanol-fed rodents, intestinal cell apoptosis increased with the degradation of tight junction protein Cho et al. In addition, the levels of bacterial endotoxins in the blood of alcoholics, alcoholic hepatitis, and liver cirrhosis patients were higher than those of healthy people Fukui et al.
The gut-derived endotoxins contribute to increased intestinal permeability and alcohol-induced tissue injury Schnabl and Brenner, Alcohol could disrupt the tight junctions of epithelial cells, which cause endotoxins translocation and the pathogenesis of ALD.
The anti-microbial peptide could be used to treat ALD. When feeding the mice with alcohol, the anti-microbial peptide REG3G expression in the intestinal tissues was reduced Wang et al.
In addition, when the mice were gavaged with the engineered bacteria which overexpress interleukin 22 IL22 to induce REG3G expression, the severity of the alcohol-induced liver injury can be reduced Hendrikx et al.
The amount of Bacteroidetes and Firmicutes was reduced, while the Proteobacteria was increased in the colon samples of ALD patients Mutlu et al. However, a higher abundance of Streptococci , Bifidobacteria , Enterobacteria , and decreased anti-inflammatory Clostridium leptum or Faecalibacterium prausnitziithan were found in feces of patients with severe alcohol-associated hepatitis than controls Llopis et al.
The dysbiosis of intestinal flora was observed in alcoholics, Enterobacteriaceae significantly increased and Bacteroidetes and Lactobacillus reduced Mutlu et al. Either alcohol withdrawal or probiotic oral supplementation could reduce alcohol-induced dysbiosis Leclercq et al.
The gut microbiota composition between patients with severe alcoholic hepatitis AH and alcoholic patients without alcoholic hepatitis non-AH are significantly different. To study the GM function on the pathology of AH.
GM was collected from AH and non-AH groups and transplanted into germ-free mice separately. In the following five weeks, mice were fed an alcohol-containing diet. The non-AH donor GM received group gained more weight than the severe AH donor group. Liver inflammation was more severe in the severe AH donor group Jefferies et al.
By gut microbiota sequence analysis, in both groups, the abundance of Bacteroides was dominant, but in severe AH mice, the number was more marked. Butyricimonas, Bilophila , Clostridium cluster XIVa and Alistipes were also more significantly abundant in the severe AH mice.
Large amount of Parasutterella excrementihominis was found in non-AH mouse microbiota, but almost absent in severe AH donors, which suggest the bacteria may have a protective effect Llopis et al. Hepatitis virus infections include chronic hepatitis B HBV and chronic hepatitis C HCV infection.
The gut microbiome is involved in the progression of hepatitis virus-related liver disease. Gut microbiota alterations were significantly associated with liver disease progression.
Compared to healthy controls, patients with HBV has a higher abundance of Veillonella , Fusobacteria , and Haemophilus , lower amount Prevotella and Phascolarctobacterium Chen et al. Primary sclerosing cholangitis is a chronic bile duct disease characterized by inflammation and bile ducts fibrosis, which leads to impaired bile formation or flow.
Most patients eventually with a high rate of cirrhosis, portal hypertension, and liver dysfunction Lazaridis and Larusso, Currently, there is no effective medical treatment for PSC, and liver transplantation is the only effective option with high cost.
Recently, a lot of research has focused on the role of gut microbiota in PSC Little et al. Sabino et al. found intestinal microbiota diversity of PSC was decreased, the number of Enterococcus , Fusobacterium , and Lactobacillus significantly increased Sabino et al.
Another study also found the bacterial diversity was reduced and the mucosa-associated bacteria an uncultured Clostridiales II was under- represented Rossen et al.
A further study concluded the number of Blautia and Barnesiellaceae were increased in the mucosal samples of PSC Torres et al. The abundance of Veillonella has been proved to be associated with PSC Iwasawa et al.
Veilonella contains genes that can encode amine oxidase, this molecule has important effects on the liver. In various studies, Veilonella appears to also have pro-inflammatory features Van den Bogert et al.
A UK study showed that the increase of Escherichia , Megasphera , Lachnospiraceae and reduction in Roseburia and Prevotella , Bacteroides was almost disappeared in PSC patients Quraishi et al. Rühlemann et al.
demonstrated eight taxa enriched in PSC compared to healthy controls. An increase of Proteobacteria and Parabacteroides were newly identified in PSC, and they are bile-tolerant taxons, which are important in cholesterol and bile acid metabolism Rühlemann et al.
Patients with PSC have a signature characterized by several genera decrease and certain genera increase, these genera could be the biomarkers for PSC and can highly predict PSC Table 1. Cirrhosis is characterized by hepatocyte loss, fibrous scar thickening, and regenerative nodules Bhat et al.
NAFLD, ALD, primary sclerosing cholangitis, and hepatitis can progress to cirrhosis Tsochatzis et al. Specific bacteria enrichment or decrease were correlated with the severity of cirrhosis Qin et al.
Spontaneous bacterial peritonitis or worsened liver dysfunction was often found in cirrhosis patients. Quin and colleagues assessed the most extensive metagenome communities of cirrhosis Qin et al.
Many studies have proved that the fecal microbial community has significant alterations in cirrhosis patients Bajaj and Khoruts, ; Zheng et al. The abundance of Fusobacteria and Proteobacteria increased whereas Bacteroidetes was significantly reduced in the cirrhosis patients Chen et al.
Another study showed Enterobacteriaceae and Enterococcus were significantly increased, the ratio of Bifidobacterium and Enterobacteriaceae were reduced in cirrhotic patients.
Plasma endotoxin, IL-6, and fecal secretory IgA were negatively correlated with Bacteroides-Prevotella group and Eubacteria group. The plasma concentration of endotoxin and IL-6 significantly increased in cirrhotic patients Liu et al. Bajaj et al. confirmed the association between GM and liver cirrhosis, which showed that GM diversity and symbiosis significantly improved in patients with severe liver cirrhosis after liver transplantation Bajaj et al.
However, Bacteroidetes , Lachnospiraceae , and Ruminococcaceae were reduced while Enterobacteriaceae , Alcaligenaceae , Streptococcaceae , Veillonellaceae , and Fusobacteriaceae were increased in cirrhosis patients when comparison with healthy controls Bajaj et al.
These findings provide a new approach for the management of liver cirrhosis with an emphasis on gut microbiota regulation. Hepatic encephalopathy HE , is a reversible neuropsychiatric impairment caused by impaired liver function.
Studies have shown that the decrease of blood hypoxia peristalsis can cause intestinal flora imbalance, thus increasing the release of intestinal ammonia and endotoxin, and inducing hepatic encephalopathy. However, the types of intestinal microbiota involved in this process are not clear.
Intestinal dysbiosis, inflammation, and oxidative stress could be observed in the pathogenesis process of HE Rai et al. The most possible pathology of HE is the damaged liver cannot convert intestinal nitrogenous toxins into non-toxic substances and excrete them from the body.
Other neurotoxins include methionine derivatives such as thiols, phenols and fatty acids, they may act synergistically with ammonia.
Food and gut-derived substances such as pseudoneurotransmitters such as octopamine, benzodiazepine ligands and GABA, are elevated in HE and have been blamed for interfering with neurotransmission. However, their significance in HE pathogenesis is unclear. The excess ammonia in the intestine is transferred to the brain and causes brain damage.
The urease-producing bacteria which can produce ammonia and endotoxins such as Proteus and Klebsiella are increased in the intestine Milosevic et al. In contrast, genera over-represented in HE Megasphaera , Enterococcus , and Burkholderia were linked to poor cognition and inflammation Bajaj et al.
When compared to cirrhotic patients without HE, a higher proportion of Veillonellaceae was observed in HE, this bacteria was associated with increased inflammatory cytokines IL-6, TNF-α, IL-2, and IL and poor cognition. The enrichment of the Alcaligenaceae family is related to poor cognitive ability.
Proteobacteria is an opportunistic pathogen that can degrade urea to ammonia, and this gives a reasonable explanation for cognitive loss Bajaj, Therefore, it has been assumed that identifying specific fecal microbial characteristics could be used to predict the absence of minimal HE, instead of cognitive testing Bajaj et al.
These findings suggest that the microbiome composition of HE patients is closely related to cognition and inflammation.
Hepatocellular carcinoma HCC is the third leading cause of high cancer mortality. Cirrhosis and viral hepatitis may progress to HCC Cabrera and Nelson, Experiments have provided evidence that gut microbiota plays a role in hepatocarcinogenesis Yu and Schwabe, Dipito et al.
found that TLR4 deletion can reduce the number and size of HCC, but cannot prevent the incidence of tumors Dapito et al. Thus, the TLR4-LPS pathway is not required for HCC initiation but HCC promotion. When the gut barrier was disrupted, LPS from the gut promotes hepatocarcinogenesis through hepatic stellate cells, hepatocyte-tumor compartment, and Kupffer cells Gupta et al.
Another critical mechanism about the LPS—TLR4 axis promotes HCC formation is through NFκBmediated pathway. Activated TLR-4 further triggers inflammatory signaling pathways for NFκB that induce the production and release of inflammatory cytokines IL-1β and IL Yu et al.
Moreover, LPS activates TLR4 in HCC cells can enhance their potential invasive ability and induce the transition of epithelial-mesenchymal Yu and Schwabe, Until now, studies conducted on the gut microbiome and different underlying liver cirrhosis, showing that at least some microbial changes have the same features to different aetiologies.
Secretion of bile reduced and changes in intestinal secretion of anti-microbial peptides and IgA at end-stage of liver disease. The common alteration of gut microbiota composition in patients with liver cirrhosis includes enrichment of Veillonella or Streptococcus and decrease of order Clostridiales Bajaj et al.
In addition, Escherichia coli were significantly increased in fecal samples of HCC patients compared to cirrhosis patients without HCC, indicating that hepatocarcinogenesis may attribute to the overgrowth of E. coli Grt et al. The most common bacteria isolated from tongue swabs of patients with HCC are Oribacterium and Fusobacterium.
On the other hand, decreases of Lactobacillus , Bifidobacterium and Enterococcus were observed in stool samples of HCC patients Zhang et al. It was also reported deoxycholic acid DCA accelerates the HCC development in obese mice by inducing the senescence-related secretory phenotype SASP in HSCs Yoshimoto et al.
In addition to synergy with DCA, lipoteichoic acid enters the liver through TLR2 and up-regulates the expression of SASP and COX-2 in senescent HSCs Loo et al.
Both gut microbiome and their metabolites play a vital role in the process of HCC, microbiome-targeted therapeutic modalities for HCC aroused great interest from scholars, and we will discuss possible approaches in detail in the next paragraph. Gut microbiota-related strategies to manage chronic liver disease were summarized in Table 2.
Table 2 Gut microbiota related strategies to manage chronic liver diseases. Many studies focus on dietary modification to optimize the structure of gut microbiota. Higher intakes of branched-chain amino acids BCAAs, leucine, isoleucine and valine and vegetable proteins have shown benefits in cirrhosis patients Fukushima et al.
BCAA-enriched diet can reduce the progression of liver failure in patients with advanced cirrhosis, which can reduce the severity and frequency of HE, and improve quality of life. Thiamine supplementation should be considered in severely alcoholic patients Satish and Shaik, Fat-soluble vitamin supplementation should be considered in conditions of cholestatic Atarashi et al.
Vitamin K supplementation is only to be considered at high risk of a hemorrhagic situation Atarashi et al. Zinc and magnesium supplementation can indirectly improve nutrient intake and nutritional status Garrett-Laster et al.
Calcium and vitamin D supplementation could be considered in patients with cholestasis and osteoporosis Francis, SCFAs regulate liver metabolism and immune function by inhibiting histone deacetylase or activating G-protein coupled receptors, including GPR41, GPR43, GPRa, and OLFR In addition, acetate and propionate have anti-inflammatory properties and inhibit hepatic lipogenesis and lipid accumulation Sahuri-Arisoylu et al.
Butyrate can modulate the GM composition, increase the expression of glucagon-like peptide-1 receptors GLP-1R , reduce inflammatory signals and liver oxide damage, ultimately attenuate steatohepatitis Jin et al. Recently, Beaumont et al. have proved that after feeding the mice with indole, the expression of tight junction protein was up-regulated, and the mice display resistance to liver inflammation Beaumont et al.
Choline deficiency in diet could lead to reversible hepatic steatosis. Choline has a function in removing fat from hepatocytes Yu et al. Metagenomic analysis of the microbial communities in the intestinal tracts of 15 women showed that increased Gammaproteobacteria and decreased Erysipelotrichi can prevent steatosis with a choline-depleted diet Spencer et al.
Antibiotics can decrease the total number of gut microbiota, eliminate bacteria with a high ability to translocate and inhibit pro-inflammatory signals arising from the gut ecosystem Zhang et al.
Rifaximin could be used to treat HE in clinical trials Kimer et al. It may increase the number of beneficial bacteria while decreasing the number of harmful bacteria, and also improve beneficial bacteria function.
Rifaximin could reduce gut-derived toxins and reduce serum pro-inflammatory cytokines levels Ponziani et al. It may also affect gut microbiota metabolites Bajaj, The research tested the functions of rifaximin on cirrhotic patients with minimal HE.
They analyzed both the structure of gut microbiota and the metabolome of serum and urine. The results showed that after eight weeks of rifaximin treatment, cognition and endotoxemia could be improved.
However, the unsaturated and saturated fatty acids in the serum were significantly increased after rifaximin treatment. The results showed rifaximin does not change the overall composition and diversity of gut microbiota, it modifies the metabolites of the bacteria.
Rifaximin can also increase the concentration of linoleic and arachidonic acids, which have brain beneficial functions Tang, Many studies have reported that probiotics have beneficial effects on liver health.
Probiotics have functions in improving nutritional stations, repairing mucosal barrier, providing short-chain acids to prevent apoptosis, improving intestinal epithelial viability Kanauchi et al.
These functions prevent the disturbance of pathogens on tight junctions. Lactobacillus GG can improve intestinal oxidative stress, intestinal leakage, and liver injury in the alcoholic steatohepatitis rat model Forsyth et al.
In patients with alcoholic cirrhosis, probiotics Lactobacillus casei Shirota may restore phagocytosis of neutrophils by changing IL secretion and TLR4 expression Stadlbauer et al. The effectiveness of probiotics on liver cirrhosis can be divided into improving liver function and preventing pathogens infection, hepatic encephalopathy, and other complications.
Intake of VSL 3 daily for six months significantly reduced the risk of hospitalization for HE and improved Child-Turcotte-Pugh CTP and model for end-stage liver disease scores MELD in patients with cirrhosis Dhiman et al. The ability of probiotics to modulate GM has therapeutic potential.
There is some evidence regarding probiotic usage to treat spontaneous bacterial peritonitis SBP and HE. Further research in evaluating gut microbiota and appropriately selected beneficial bacterial strains as treatment modalities should be undertaken Forsyth et al.
Prebiotics are non-digestible but fermentable food substances fermented by bacteria and help the intestine peristaltic and selectively stimulate the growth of gut bacteria. Some prebiotic foods, like lactulose and pectin, seemed to be promising therapeutic agents to treat liver diseases.
Lactulose is an unabsorbable disaccharide, which can acidify the intestinal cavity, inhibit urease-producing bacteria, and limit the diffusion of ammonia into the blood Phongsamran et al. The main treatment for HE patients is to target the intestine to reduce colonic bacterial generation and reduce blood ammonia.
Pectin can restore the levels of Bacteroides and prevent liver damage in rodent models Ferrere et al. A meta-analysis of NAFLD patients showed significant reductions in BMI, liver enzymes, serum cholesterol, and triglycerides after prebiotic treatment. This suggests that prebiotics may improve NAFLD by regulating intestinal flora homeostasis Loman et al.
Fructooligosaccharide FOS can promote fatty acid oxidation by up-regulating peroxidase expression, inhibiting the expression of SREBP-2 in the liver, and reducing the accumulation of cholesterol Matsumoto et al. This showed oligosaccharides could reduce bacterial overgrowth and improve alcoholic steatohepatitis by restoring the expression of partial lectin protein reg3g.
Lactulose is prebiotic which can promote the growth of Bifidobacterium and Lactobacillus. Fan et al. used lactulose to treat NASH mice.
Symbiotics consist of a combination of probiotics and prebiotics. Symbiotics have the function of regulating the expression of intestinal flora and related functional genes.
It can reduce the colitis reaction and liver inflammatory response, reduce the level of SCFA in feces, enhance tight junction of the intestinal barrier, and improve fatty degeneration of the liver as well as insulin resistance.
Meanwhile, symbiotics can reduce the degree of liver fibrosis and LPS in mice. Clinical research indicated that after six months of intervention by Bifidobacterium longum and FOS in 66 NASH patients, serum AST, LPS, and inflammatory response transmitters HOMA-IR , fat denaturation and NASH activity index were significantly reduced Malaguarnera et al.
Symbiotic treatment could be an ideal approach to treat liver diseases since they can protect against inflammation and hepatocyte damage through probiotics and prebiotics. The mechanism of symbiotic protection has not yet been fully clarified. Potential mechanisms of symbiotic effect on liver disease include gut microbiota structure and microbiota metabolite alteration, which have anti-inflammatory and immunomodulatory effects.
There are no adverse effects that have been reported with this approach. Fecal microbiota transplantation FMT means transplanting bacteria from the feces of healthy individuals into the recipient through a series of routes Xu et al.
FMT can restore the health of intestinal flora, further reduce the transport of endogenous ethanol, endotoxin, and other metabolites to the liver, reduce the damage of metabolic substances to the liver, and also effectively reduce the inflammatory response and the expansion of liver cells.
Compared with the oral probiotics method, FMT can significantly improve intestinal bacteria disorder, and FMT is the most effective method to restore intestinal microecological balance currently.
FMT has been studied more deeply in recent years. The possible mechanism of FMT involves establishing beneficial microbes in the gut and the production of anti-microbial substances. The number of Bacteroides in alcohol-sensitive mice decreased, and the number of Actinobacteria and Firmicutes increased.
Alcohol-sensitive mice had fifty percent fewer Bacteroides than alcohol-resistant mice Ferrere et al. Zhou et al. used fecal bacteria transplantation to treat NAFLD mice caused by a high-fat diet.
The results showed that fecal bacteria transplantation could improve intestinal flora disorder, enhance intestinal barrier function and reduce liver steatosis Zhou et al. At present, FMT has successfully treated Clostridium difficile infection patients in clinical and promoted the recovery of intestinal ecological balance.
Simultaneously, the clinical results showed that the improvement effect was better than that of standard antibiotics. A clinical trial showed that FMT showed good safety in 10 patients with primary sclerosing cholangitis complicated with IBD, and it could effectively reduce alkaline phosphatase in some patients.
Liver enzymes, fecal microflora, and fecal metabonomics were analyzed at 1, 4, 8, 12, and 24 weeks after FMT.
FMT rarely has adverse events. Therefore, FMT can be used as an effective method to treat and prevent chronic liver disease. The preliminary basic research shows that FMT can restore the probiotics in the intestinal ecosystem Craven et al. Therefore, fecal bacteria transplantation could be a valuable and safe treatment for cirrhosis.
The advantage of FMT is that it can rebulid the whole dysbiotic intestinal environment, but the best optimal route of administration, the duration of treatment and the durability of reaction still need to be determined.
There is an urgent need for large-scale and high-quality research in this field in order to evaluate the most effective method to achieve rebiosis. The gut microbiota plays an important role in the pathogenesis of chronic liver diseases, including NAFLD, ALD, Hepatitis Virus Infection, PCS, cirrhosis, and HE.
The mechanism of connection between liver diseases and the intestine is poorly understood. Intestinal permeability is closely related to chronic liver disease. The increase of intestinal permeability will lead to the release of intestinal inflammation factors and cause flora dysbiosis, which contributes to liver disease development Fukui, The liver can communicate with the gut through bile acids circulation.
The binding of BAs to FXR can induce anti-microbial peptides to produce, which can inhibit gut microbial overgrowth and improve gut barrier function. Choline assists the liver in excreting VLDL particles, preventing the accumulation of triglycerides in hepatic steatosis.
Intestinal bacteria can convert choline into TMA. TMA can be transferred to the liver and converted to TMAO, which is associated with liver injury. Gut microbiota also can produce SCFAs including butyrate, propionate, acetate, etc. Butyrate can reduce intestinal permeability and subsequent liver injury induced by alcohol.
Since the gut microbiota places an important role in the progress of the chronic liver disease, we believe the gut-microbiota-targeted interventions could be used to regulate the intestinal flora community and manage chronic liver diseases.
However, a comprehensive understanding of the interactions between microbes and liver diseases is still not clear. Although animal models help to elucidate many important mechanistic pathways in the etiology of liver diseases.
From animal models to human models requires well-designed, large-scale clinical trials spanning multiple disease aetiologies and patient characteristics. With the increasing recognition of the role of the microbiome in the development, prognosis, and treatment of liver diseases, we emphasize the need for a focus on the microbiome to effectively address the socioeconomic burden of this type of liver disease.
Furthermore, it is critical to use animal models that mimic human disease as closely as possible. JL contributed to manuscript writing. DY, XW, QZ, and LN critically reviewed the manuscript. PA critically edited the English in the manuscript.
LS supervised the whole process and reviewed the manuscript. All authors contributed to the article and approved the submitted version.
This research was financially supported by the Natural Science Foundation of Shanghai 20ZR , the National Natural Science Foundation of China , Shanghai Excellent Technology Leader Program 17XD , Shanghai Municipal Public Health System Construction Three-Year Action Plan GWV The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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The gut-liver axis is the communication between the Liver health and gut health connection, Essential vitamin sources microbiome but the ght. Research into the relationship between the gut and liver Lievr important for human health. Here we explore the connections between these two important organs. The liver and the intestine are anatomically linked. The liver gets most of its blood flow from the intestine. This blood flow enables the transport of nutrients from the food we eat to the liver. The liver is the key metabolic organ of the body that produces and sends off metabolites to the whole body.The jealth system allows continuous communication and interaction gur these three important organs. This healhh Liver health and gut health connection the healt body health of an individual Lver well as the functionality of the body.
Latest research confirms the working of gut-liver-brain axis in a manner heslth influences our mental health haelth well as other Liver health and gut health connection workings healht the Livsr.
We will explore the detailed Liver health and gut health connection relationships with Nutrition for young athletes axis while Livfr light on how our gut influences the liver function and presses our connfction health in a certain manner.
It Lier us against heslth infections connectiob harmful substances in the body. This critical function is achieved gyt the znd of Maintaining a balanced gut important nutrients after blocking the unwanted substances present Liiver food.
This is also conhection after Easy quinoa recipes toxins heakth bacteria in the bloodstream. An helath gut healty cause gaps in its boundaries anv allows heallth toxins to gather in the body. This will also allow various kinds of bacteria to enter, stay and Liver health and gut health connection the body.
Furthermore, anf act ane degrade connectioh functionality of the liver while unleashing connectiln cascade Liver health and gut health connection cnnection tissues. More about the xnd relationship is Liver health and gut health connection balance of gut wakefulness and daytime fatigue. It Liver health and gut health connection healthh massive community of microorganisms Elevates mood naturally the digestive tract.
When balanced, this ecosystem can promote great health and harmonious liver function. Similarly, disturbances in this ecosystem can cause disruptive liver health.
An imbalance in this ecosystem is always linked with liver dysfunction, inflammation and various liver diseases. The gut-brain axis is a notable communication network that interlinks the gut and the brain through several pathways.
This consists of the nervous system and chemical signalling. This axis also offers a dynamic bridge between our gastrointestinal system and our mental health which reveals an interesting connection.
Influence on mood levels, emotions and mental health can be caused due to the condition of an unhealthy mental health which signals the brain to act in a certain way. It is a neurotransmitter that contributes to the positivity of mental well-being.
An unhealthy gut can reduce the production of serotonin causing anxiety and depression. The liver and brain connection is called the liver-brain axis. They have the ability to send signals back and forth.
The liver cleanses the body and regulates it whereas the brain tells the liver what to perform and what not to perform. The liver also regulates various functions like energy balance, glucose metabolism, lipid metabolism and detoxification. When this overall system between the liver and the brain is imbalanced, a lot of mess is caused.
It can develop issues like problems with how the body utilises energy, brain diseases and even mental health problems. Therefore, it is extremely important for the liver and the brain to communicate well. It keeps the body healthy and balanced in all the possible ways. Identifying and detecting such problems as early as possible can result in higher rates of survival of an individual.
If not, it may even cause death or degradation of the body eventually. This blog has been converted from the PR article - What Is The Gut-Liver-Brain Axis? Know How Your Gut Impacts Liver Function And Mental Health. Facebook Twitter instagram Youtube.
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: Liver health and gut health connection| Minding the Gut-Liver-Brain Connection: Revolutionizing Your Well-Bein | A Note on Your Heealth. Schnabl, B. Emerging connecgion of Liver health and gut health connection hydrocarbon Essential nutrients for athletes in Livrr altered clearance of connrction during Liver health and gut health connection kidney disease. It promotes regular heatlh movements and reduces constipation. A brand new placebo-controlled clinical trial read about it here — just published in April — showed that probiotic supplements brought significant improvements to obese patients with NAFLD. Open Access This article is licensed under a Creative Commons Attribution 4. Prebiotics are non-digestible but fermentable food substances fermented by bacteria and help the intestine peristaltic and selectively stimulate the growth of gut bacteria. |
| The liver’s letters to the gut – bile acids | Bidirectional Communication Between Liver and Gut During Alcoholic Liver Disease. The increase in TMAO levels is associated to liver as well as CV events Content , 31—36 Thiamine supplementation should be considered in severely alcoholic patients Satish and Shaik, Naiara Beraza. |
| Want to Be Healthier? First Look to Your Gut – Veracity Selfcare | Article CAS PubMed Google Scholar Loomba, R. Article CAS PubMed Google Scholar Filliol, A. Proteobacteria is an opportunistic pathogen that can degrade urea to ammonia, and this gives a reasonable explanation for cognitive loss Bajaj, Made with 💙. Association Between Composition of the Human Gastrointestinal Microbiome and Development of Fatty Liver With Choline Deficiency. On the other side of the equation are the things your body needs to get rid of, like the toxins you ingest from food, air, and water or the hormones that have been broken down and are no longer needed. |
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Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature , 57—63 Geng, J. Fukami, K. Oral L-carnitine supplementation increases trimethylamine-N-oxide but reduces markers of vascular injury in hemodialysis patients. Gao, X. Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice. Download references. We thank TCS research for their constant support. We also acknowledge pixabay for some of the copyright free images used in this manuscript. TCS Research, Tata Consultancy Services Ltd, Pune, , India. You can also search for this author in PubMed Google Scholar. and S. designed the review and drafted the manuscript. Both authors approved the final version of the manuscript for submission. Correspondence to Swadha Anand or Sharmila S. are employed by company Tata Consultancy Services Ltd. Both authors declare no competing interests. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Host-microbiome interactions: Gut-Liver axis and its connection with other organs. npj Biofilms Microbiomes 8 , 89 Download citation. Received : 27 September Accepted : 18 October Published : 01 November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Reviews in Endocrine and Metabolic Disorders By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature. nature npj biofilms and microbiomes review articles article. Your Email. Andy De Santis MPH, RD DR. RD ARCHIVE. Exploring Acid Reflux-Friendly Coffee Alternatives. IBS-Friendly Workdays: Conquer Deskbound Life with Health and Activity. Mastering Gut Health: How Diet Influences Your Microbiome. Crafting the Ultimate Gluten-Free Pizza Crust RECIPE INSIDE. Hiatal Hernia and Its Impact on GERD. Seeking Professional Help: Couples Therapy for IBS Support. if you already know what you're looking for, try visiting a section of the site first to see A-Z listings. They believe that this diet will stimulate a type of gut bacteria called Blautia producta, which produces a byproduct which causes liver injury. Li, Staveley-O'Carroll and fellow co-principal investigator R. Scott Rector, PhD , the Director of NextGen Precision Health Building and Interim Senior Associate Dean for Research — are part of NextGen Precision Health, an initiative to expand collaboration in personalized health care and the translation of interdisciplinary research for the benefit of society. 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