Molecular Mechanisms of Alcoholic Fatty Liver

Purohit, Vishnudutt; Gao, Bin; Song, Byoung‐Joon

doi:10.1111/j.1530-0277.2008.00827.x

Cited by 312Alcohol Consumption and Health EffectsLiver Disease Diagnosis and TreatmentLiver physiology and pathology

Molecular Mechanisms of Alcoholic Fatty Liver

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Purohit, Vishnudutt, Gao, Bin, Song, Byoung‐Joon·2009·Alcoholism: Clinical and Experimental Research

DOI 10.1111/j.1530-0277.2008.00827.xPMC PMC2633431

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Abstract

Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. Alcohol exposure may induce fatty liver by increasing NADH/NAD+ratio, increasing sterol regulatory element‐binding protein‐1 (SREBP‐1) activity, decreasing peroxisome proliferator‐activated receptor‐α (PPAR‐α) activity, and increasing complement C3 hepatic levels. Alcohol may increase SREBP‐1 activity by decreasing the activities of AMP‐activated protein kinase and sirtuin‐1. Tumor necrosis factor‐α (TNF‐α) produced in response to alcohol exposure may cause fatty liver by up‐regulating SREBP‐1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down‐regulating SREBP‐1 activity. PPAR‐α agonists have potentials to attenuate alcoholic fatty liver. Adiponectin and interleukin‐6 may attenuate alcoholic fatty liver by up‐regulating PPAR‐α and insulin signaling pathways while down‐regulating SREBP‐1 activity and suppressing TNF‐α production. Recent studies show that paracrine activation of hepatic cannabinoid receptor 1 by hepatic stellate cell‐derived endocannabinoids also contributes to the development of alcoholic fatty liver. Furthermore, oxidative modifications and inactivation of the enzymes involved in the mitochondrial and/or peroxisomal β‐oxidation of fatty acids could contribute to fat accumulation in the liver.

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Ethanol metabolism primarily occurs in the liver in three major steps: ethanol oxidation to acetaldehyde, acetaldehyde metabolism to acetate, and acetate catabolism to H2O and CO2.
“Ethanol metabolism primarily occurs in the liver in three major steps: (1) ethanol oxidation to acetaldehyde, (2) acetaldehyde metabolism to acetate, and (3) acetate catabolism to H2O and CO2132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
Cytosolic ADH is a major enzyme that catalyzes oxidative metabolism of ethanol to acetaldehyde by using NAD+ converted to NADH.
“Cytosolic ADH is a major enzyme that catalyzes the oxidative metabolism of ethanol to acetaldehyde by using the cofactor nicotinamide adenine dinucleotide (NAD+) converted to NADH132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
Catalase may participate in ethanol oxidation in the presence of H2O2 but appears to play no major role in hepatic ethanol metabolism under physiological conditions due to limited H2O2 supply.
“Catalase present in peroxisomes may participate in ethanol oxidation in the presence of H2O2132–134, although this enzyme appears to play no major role in hepatic ethanol metabolism under physiological conditions due to the limited supply of H2O2135.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
Acetate produced is further degraded to CO2 and H2O, ending the final step of ethanol oxidation in the liver.
“Finally, the acetate that is produced is further degraded to CO2 and H2O, ending the final step of ethanol oxidation in the liver132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
Continued mitochondrial dysfunction with increased oxidative stress sensitizes hepatocytes to subsequent necrosis and/or apoptosis, which likely leads to activation of Kupffer cells and recruitment of infiltrating immune cells with elevated hepatic inflammation and pro-inflammatory cytokines/chemokines.
“Continued mitochondrial dysfunction with increased oxidative stress also sensitizes the hepatocytes to subsequent necrosis and/or apoptosis of hepatocytes, which likely lead to activation of resident liver macrophage (i.e., Kupffer cells) and recruitment of infiltrating immune cells into the liver with elevated levels of hepatic inflammation (steatohepatitis) and pro-inflammatory cytokines/chemok”
From Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications (2014) · cites this paper as [13]

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Alcoholic liver disease
Seitz, H. K., Bataller, R., Cortez-Pinto, H., Gao, B., Gual, A., Lackner, C., Mathurin, P., Mueller, S., Szabo, G., & Tsukamoto, H. (2018) · Nature Reviews Disease Primers · doi:10.1038/s41572-018-0014-7 · Cited by 1,271 · see citing works
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Authors: Purohit, V., Gao, B., & Song, B.
Affiliations: National Institutes of Health (US)
Corresponding author: Purohit, Vishnudutt
ORCID: Gao, Bin
Song, Byoung‐Joon
Venue: Alcoholism: Clinical and Experimental Research
Publisher: Wiley
Published: 2009-01-22
Volume: 33
Issue: 2
Pages: 191-205
ISSN: 0145-6008 (ISSN-L)
1530-0277
DOI: 10.1111/j.1530-0277.2008.00827.x
PMC: PMC2633431
OpenAlex: W2066238144
Cited by: 312
References: 214
Citations by year: 2026: 5 · 2025: 9 · 2024: 18 · 2023: 18 · 2022: 12 · 2021: 16 · 2020: 17 · 2019: 20 · 2018: 14 · 2017: 20 · 2016: 17 · 2015: 24 · 2014: 26 · 2013: 16 · 2012: 28
FWCI: 2.03
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Alcoholism Clinical and Experimental Research (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (Z99‐AA999999, Z99 DA999999)
National Institute on Alcohol Abuse and Alcoholism (Z01AA000036)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: alcoholic fatty liver, steatohepatitis, liver fibrosis, liver cirrhosis, SREBP1, PPARα, NAD+/NADH ratio, AMPK, SIRT1, TNF-α, complement C3, betaine, pioglitazone, adiponectin, interleukin-6, insulin signaling, hepatic stellate cells, CB1 receptor, endocannabinoids, fatty acid beta-oxidation, oxidative modification, hepatic lipid accumulation
MeSH terms: Animals, Complement C3, Fatty Liver, Alcoholic, Humans, NAD, Tumor Necrosis Factor-alpha, PPAR alpha, Sterol Regulatory Element Binding Proteins

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Molecular Mechanisms of Alcoholic Fatty Liver

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