Letter to the Editor: Moderate Alcohol Use in Fatty Liver Disease: Don’t Throw the Cabernet Out With the Bathwater

Gow, Paul J; Testro, Adam; Hey, Penelope; Sinclair, Marie

doi:10.1002/hep.31049

Cited by 3 publications

(3 citation statements)

References 4 publications

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“…Although alcohol consumption and NAFLD commonly exist, the data on the effects of moderate alcohol drinking on NAFLD progression remain controversial [73][74][75][76]. Data from the National Health and Nutrition Examination Survey conducted from 1988 to 2010 revealed that modest alcohol consumption (0.5-1.5 drinks or 7-21 g/day) is associated with decreased mortality among patients with NAFLD [73].…”

Section: Aldh2 and Non-alcoholic Fatty Liver Disease (Nafld)mentioning

confidence: 99%

Aldehyde Dehydrogenase, Liver Disease and Cancer

Wang

et al. 2020

Int. J. Biol. Sci.

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Acetaldehyde dehydrogenase 2 (ALDH2) is the key enzyme responsible for metabolism of the alcohol metabolite acetaldehyde in the liver. In addition to conversion of the acetaldehyde molecule, ALDH is also involved in other cellular functions. Recently, many studies have investigated the involvement of ALDH expression in viral hepatitis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), liver fibrosis, and liver cancer. Notably, ALDH2 expression has been linked with liver cancer risk, as well as pathogenesis and prognosis, and has emerged as a promising therapeutic target. Of note, approximately 8% of the world's population, and approximately 30-40% of the population in East Asia carry an inactive ALDH2 gene. This review summarizes new progress in understanding tissue-specific acetaldehyde metabolism by ALDH2 as well as the association of ALDH2 gene polymorphisms with liver disease and cancer. New research directions emerging in the field are also briefly discussed.

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Section: Aldh2 and Non-alcoholic Fatty Liver Disease (Nafld)mentioning

confidence: 99%

Aldehyde Dehydrogenase, Liver Disease and Cancer

Wang

et al. 2020

Int. J. Biol. Sci.

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“…A study involving Chinese adults revealed that the intake of alcohol and high-carbohydrate diet was positively associated with NAFLD incidence [ 96 ]. However, another study revealed that moderate alcohol consumption might reduce liver fibrosis and mortality due to NAFLD [ 97 ]. Combining fructo-oligosaccharide with silybin treatment has been shown to enhance therapeutic effects on NAFLD by modulating the intestinal micro-ecological balance and reducing the mouse body weight [ 98 ].…”

Section: Discussion: Regulatory Effects Of Bioactive Compounds From P...mentioning

confidence: 99%

Pharmacology of bioactive compounds from plant extracts for improving non-alcoholic fatty liver disease through endoplasmic reticulum stress modulation: A comprehensive review

Huang,

Tan,

et al. 2024

Heliyon

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“…1,2 Several clinical studies have documented the additive effects of obesity and heavy/moderate alcohol drinking on steatohepatitis and liver-related death. [8][9][10][11][12][13] For example, in a cohort study of 233 alcoholic hepatitis patients, obesity was found to be associated with a greater than two-fold increase in short-term mortality. 2 However, the clinical data on the effects of light to moderate alcohol drinking on NAFLD have been controversial.…”

Section: Clinical Data On the Effects Of Obesity And Alcohol Drinkingmentioning

confidence: 99%

Obesity and binge alcohol intake are deadly combination to induce steatohepatitis: A model of high-fat diet and binge ethanol intake

2020

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Obesity and binge drinking often coexist and work synergistically to promote steatohepatitis; however, the underlying mechanisms remain obscure. In this mini-review, we briefly summarize clinical evidence of the synergistical effect of obesity and heavy drinking on steatohepatitis and discuss the underlying mechanisms obtained from the study of several mouse models. High-fat diet (HFD) feeding and binge ethanol synergistically induced steatohepatitis and fibrosis in mice with significant intrahepatic neutrophil infiltration; such HFD-plus-ethanol treatment markedly up-regulated the hepatic expression of many chemokines with the highest fold (approximately 30-fold) induction of chemokine (C-X-C motif) ligand 1 (<i>Cxcl1</i>), which contributes to hepatic neutrophil infiltration and liver injury. Furthermore, HFD feeding activated peroxisome proliferator-activated receptor gamma that subsequently inhibited CXCL1 upregulation in hepatocytes, thereby forming a negative feedback loop to prevent neutrophil overaction; whereas binge ethanol blocked this loop and then exacerbated CXCL1 elevation, neutrophil infiltration, and liver injury. Interestingly, inflamed mouse hepatocytes attracted neutrophils less effectively than inflamed human hepatocytes due to the lower induction of CXCL1 and the lack of the interleukin (IL)-8 gene in the mouse genome, which may be one of the reasons for difficulty in development of mouse models of alcoholic steatohepatitis and nonalcoholic steatohepatitis (NASH). Hepatic overexpression of <i>Cxcl1</i> and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed mice by inducing neutrophil infiltration, oxidative stress, hepatocyte death, fibrosis, and p38 mitogen-activated protein kinase activation. Collectively, obesity and binge drinking synergistically promote steatohepatitis via the induction of CXCL1 and subsequent hepatic neutrophil infiltration.

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Letter to the Editor: Moderate Alcohol Use in Fatty Liver Disease: Don’t Throw the Cabernet Out With the Bathwater

Cited by 3 publications

References 4 publications

Aldehyde Dehydrogenase, Liver Disease and Cancer

Aldehyde Dehydrogenase, Liver Disease and Cancer

Pharmacology of bioactive compounds from plant extracts for improving non-alcoholic fatty liver disease through endoplasmic reticulum stress modulation: A comprehensive review

Obesity and binge alcohol intake are deadly combination to induce steatohepatitis: A model of high-fat diet and binge ethanol intake

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