Gut microbiota in non‐alcoholic fatty liver disease and alcohol‐related liver disease: Current concepts and perspectives

Arab, Juan Pablo; Arrese, Marco; Shah, Vijay H.

doi:10.1111/hepr.13473

Cited by 43 publications

(32 citation statements)

References 178 publications

(203 reference statements)

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“…Gut–liver axis signaling pathways, such as microbiota-related mechanisms (i.e., dysbiosis, production of endogenous ethanol, and choline deficiency) play a major role in the pathogenesis of NAFLD and NASH [ 71 ]. This may occur either directly or indirectly (i.e., via altered metabolism of bile acids) and is deemed to be a key element of personalized medicine [ 44 , 72 , 73 ]. Indeed, lifestyle changes are closely linked with modulation of the intestinal microbiota, which may potentially account for the inter-individual variability of patients with NAFLD [ 72 ].…”

Section: Diagnosismentioning

confidence: 99%

Perspectives on Precision Medicine Approaches to NAFLD Diagnosis and Management

Lonardo¹,

Arab

Arrese

2021

Adv Ther

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Precision medicine defines the attempt to identify the most effective approaches for specific subsets of patients based on their genetic background, clinical features, and environmental factors. Nonalcoholic fatty liver disease (NAFLD) encompasses the alcohol-like spectrum of liver disorders (steatosis, steatohepatitis with/without fibrosis, and cirrhosis and hepatocellular carcinoma) in the nonalcoholic patient. Recently, disease renaming to MAFLD [metabolic (dysfunction)-associated fatty liver disease] and positive criteria for diagnosis have been proposed. This review article is specifically devoted to envisaging some clues that may be useful to implementing a precision medicine-oriented approach in research and clinical practice. To this end, we focus on how sex and reproductive status, genetics, intestinal microbiota diversity, endocrine and metabolic status, as well as physical activity may interact in determining NAFLD/ MAFLD heterogeneity. All these factors should be considered in the individual patient with the aim of implementing an individualized therapeutic plan. The impact of considering NAFLD heterogeneity on the development of targeted therapies for NAFLD subgroups is also extensively discussed.

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Section: Diagnosismentioning

confidence: 99%

Perspectives on Precision Medicine Approaches to NAFLD Diagnosis and Management

Lonardo¹,

Arab

Arrese

2021

Adv Ther

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“…Thus, much effort has been made to improve the understanding of the pathophysiological mechanisms implicated in the development of NAFLD and NASH. Emerging mechanisms such as the involvement of the gut–liver axis–link have been discussed [ 28 , 29 ]. However, enhanced hepatic lipid accumulation, oxidative stress and inflammation remain the foremost pillars in the pathogenesis of NAFLD [ 29 ].…”

Section: A Brief Overview On Nafld and Implicated Pathophysiologicmentioning

confidence: 99%

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

et al. 2020

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Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease (NAFLD). There are currently no specific protective drugs against NAFLD, and effective interventions involving regular exercise and healthy diets have proved difficult to achieve and maintain. Alternatively, due to its antioxidant and anti-inflammatory properties, there has been growing interest in understanding the therapeutic effects of N-acetyl cysteine (NAC) against metabolic complications, including NAFLD. Here, reviewed evidence suggests that NAC blocks hepatic lipid accumulation in preclinical models of NAFLD. This is in part through the effective regulation of a fatty acid scavenger molecule (CD36) and transcriptional factors such as sterol regulatory element-binding protein (SREBP)-1c/-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Importantly, NAC appears effective in improving liver function by reducing pro-inflammatory markers such as interleukin (IL)-6 IL-1β, tumour necrosis factor alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). This was primarily through the attenuation of lipid peroxidation and enhancements in intracellular response antioxidants, particularly glutathione. Very few clinical studies support the beneficial effects of NAC against NAFLD-related complications, thus well-organized randomized clinical trials are still necessary to confirm its therapeutic potential.

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“…Additionally, the gut microbiota plays an important role in both nonalcoholic fatty liver disease and alcohol-related liver disease [ 25 ]. Alcohol may affect glucose metabolism in the liver by downregulating gluconeogenesis or changing hepatic lipids, inflammatory response, and oxidative stress by inducing steatosis [ 26 , 27 ]. It may also affect gut microbiota diversity and interfere with the protective effect of beneficial bacteria [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Serum Glycated Albumin Levels Are Affected by Alcohol in Men of the Jinuo Ethnic Group in China

Zhu

Hou

et al. 2021

Canadian Journal of Infectious Diseases and Medical Microbiolog

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Aim. To investigate the effects of alcohol on serum glycated albumin (GA) levels in Chinese men. Methods. A total of 2314 male subjects from the Jinuo ethnic group in China were enrolled. Of these, 986 subjects drank alcohol frequently and 404 subjects did not. Lifestyle information was gathered by using a questionnaire, and measurements of blood pressure, body mass index, blood glucose level, liver function, and kidney function were collected. GA was measured by using an enzymatic method. Frequent drinking was defined as a history of drinking ethanol > 80 g/d within the past two weeks. Nondrinking was defined as no alcohol consumption in the past three months. Subjects with an alcohol intake between 0 and 80 g/d in the past two weeks were included in the drinking-occasionally group. Analysis of variance (ANOVA), correlation analysis, and linear regression were used to evaluate the effects of drinking on serum GA levels. Decision tree regression (DTR) algorithm was used to evaluate the effect of features (variables) on GA levels. Results. We found that male subjects who drank frequently had significantly lower serum GA levels than subjects who did not drink (13.0 ± 1.7 vs. 14.1 ± 3.7, p < 0.05 ). Spearman’s correlation analysis calculated a coefficient of −0.152 between drinking and GA ( p < 0.005 ). Linear regression established that drinking was an independent predictor for GA levels with a standardized regression coefficient of −0.144 ( p < 0.05 ). Decision tree regression showed that the effect of drinking on GA levels (0.0283) is five times higher than that of smoking (0.0057). Conclusions. Frequent alcohol consumption could result in decreased GA levels in men of the Jinuo ethnic group in China.

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Gut microbiota in non‐alcoholic fatty liver disease and alcohol‐related liver disease: Current concepts and perspectives

Cited by 43 publications

References 178 publications

Perspectives on Precision Medicine Approaches to NAFLD Diagnosis and Management

Perspectives on Precision Medicine Approaches to NAFLD Diagnosis and Management

N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

Serum Glycated Albumin Levels Are Affected by Alcohol in Men of the Jinuo Ethnic Group in China

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