Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena, Sudheer K.; King, Adrienne L.; Andringa, Kelly K.; Eccleston, Heather B.; Bailey, Shannon M.

doi:10.1016/j.freeradbiomed.2007.12.029

Cited by 429Liver Disease Diagnosis and TreatmentAlcohol Consumption and Health EffectsMitochondrial Function and Pathology

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

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Mantena, Sudheer K., King, Adrienne L., Andringa, Kelly K., Eccleston, Heather B., Bailey, Shannon M.·2008·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2007.12.029PMC PMC2323912

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Abstract

Fatty liver disease associated with chronic alcohol consumption or obesity/type 2 diabetes has emerged as a serious public health problem. Steatosis, accumulation of triglyceride in hepatocytes, is now recognized as a critical "first-hit" in the pathogenesis of liver disease. It is proposed that steatosis "primes" the liver to progress to more severe liver pathologies when individuals are exposed to subsequent metabolic and/or environmental stressors or "second-hits." Genetic risk factors can also influence the susceptibility to and severity of fatty liver disease. Furthermore, oxidative stress, disrupted nitric oxide (NO) signaling, and mitochondrial dysfunction are proposed to be key molecular events that accelerate or worsen steatosis and initiate progression to steatohepatitis and fibrosis. This review article will discuss the following topics regarding the pathobiology and molecular mechanisms responsible for fatty liver disease: (1) the "two-hit" or "multi-hit" hypothesis, (2) the role of mitochondrial bioenergetic defects and oxidant stress, (3) the interplay between NO and mitochondria in fatty liver disease, (4) genetic risk factors and oxidative stress-responsive genes, and (5) the feasibility of antioxidants for treatment.

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Chronic alcohol consumption inhibits AMP kinase and activates sterol regulatory element binding protein-1, which increase lipogenesis resulting in hepatic steatosis.
“Chronic alcohol consumption inhibits AMP kinase and activates sterol regulatory element binding protein-1, which increase lipogenesis resulting in hepatic steatosis (Mantena et al., 2008).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Mantena et al., 2008
Hyperinsulinemia and peripheral lipolysis promote hepatic uptake of fatty acids as well as fatty acid synthesis, resulting in accumulation of fat and fatty liver.
“Hyperinsulinemia and peripheral lipolysis promote hepatic uptake of fatty acids as well as fatty acid synthesis, resulting in accumulation of fat and fatty liver (Mantena et al., 2008).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Mantena et al., 2008
Hepatic mitochondrial abnormalities are observed in both alcoholic fatty liver disease (AFLD), nonalcoholic fatty liver disease (NAFLD) and acute liver injury.
“Hepatic mitochondrial abnormalities are observed in both alcoholic fatty liver disease (AFLD) [4], [5], [6], nonalcoholic fatty liver disease (NAFLD) [7], [8], [9] and acute liver injury.”
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 [5]

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Authors: Mantena, S. K., King, A. L., Andringa, K. K., Eccleston, H. B., & Bailey, S. M.
Affiliations: University of Alabama at Birmingham (US)
Corresponding author: Bailey, Shannon M.
ORCID: King, Adrienne L.
Bailey, Shannon M.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2008-04
Volume: 44
Issue: 7
Pages: 1259-1272
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2007.12.029
PMC: PMC2323912
OpenAlex: W1977194186
Cited by: 429
References: 198
Citations by year: 2026: 10 · 2025: 16 · 2024: 20 · 2023: 11 · 2022: 22 · 2021: 21 · 2020: 24 · 2019: 24 · 2018: 26 · 2017: 27 · 2016: 24 · 2015: 26 · 2014: 32 · 2013: 20 · 2012: 31
FWCI: 3.38
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Alcohol Abuse and Alcoholism (AA15172, R01AA015172)
National Institute of Diabetes and Digestive and Kidney Diseases (R21DK073775, DK73775)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: hepatic steatosis, alcoholic liver disease, obesity, type 2 diabetes, mitochondrial dysfunction, oxidative stress, steatosis, two-hit hypothesis, nitric oxide signaling, mitochondrial bioenergetics, steatohepatitis, liver fibrosis, genetic risk factors, antioxidants
MeSH terms: Alcohols, Animals, Antioxidants, Fatty Acids, Fatty Liver, Fibrosis, Free Radicals, Humans, Mitochondria, Models, Biological, Obesity, Oxidative Stress, Disease Progression, Hepatocytes, Proteomics

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Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

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