Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites†

Neuschwander‐Tetri, Brent A.

doi:10.1002/hep.23719

Cited by 1,077Liver Disease Diagnosis and TreatmentDiet, Metabolism, and DiseaseAlcohol Consumption and Health Effects

Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites†

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Neuschwander‐Tetri, Brent A.·2010·Hepatology

DOI 10.1002/hep.23719

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Abstract

A significant body of evidence now forces us to rethink the causes of NASH. Once thought to be a disease caused by triglyceride accumulation in hepatocytes with subsequent oxidant stress and lipid peroxidation causing inflammation and fibrosis, new data from animal studies and a limited number of human studies now provide convincing evidence that triglyceride accumulation does not cause insulin resistance or cellular injury in the liver. The lipotoxic liver injury hypothesis for the pathogenesis of NASH suggests that we need to focus our therapeutic efforts on reducing the burden of fatty acids going to the liver or being synthesized in the liver. This can be accomplished by improving insulin sensitivity at the level of adipose tissue to prevent inappropriate peripheral lipolysis and by preventing unnecessary de novo lipogenesis in the liver. Excess carbohydrates are the major substrates for de novo lipogenesis, and thus, reducing carbohydrate consumption through dietary changes and increasing muscle glucose uptake through exercise remain important cornerstones of treatment and prevention of lipotoxic liver injury, a disease hitherto called NASH.

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NASH may be grossly viewed as an influx problem due to increased fatty acid load with consecutive lipotoxicity.
“NASH may therefore be grossly viewed as an influx problem due to increased fatty acid load with consecutive lipotoxicity,11 12”
From Novel therapeutic targets for cholestatic and fatty liver disease (2022) · cites this paper as [11]
Fatty acid-induced lipotoxicity results in cellular stress of hepatocytes, cholangiocytes and HSCs.
“Fatty acid (FA)-induced lipotoxicity results in cellular stress of hepatocytes,11 but also cholangiocytes25 and HSCs.26”
From Novel therapeutic targets for cholestatic and fatty liver disease (2022) · cites this paper as [11]

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“Fructose enters the glycolytic pathway to fatty acid synthesis downstream from phosphofructokinase, the rate-limiting enzyme for this pathway, and thus fructose provides an unregulated source of acetyl-CoA as the substrate for DNL.84,85 Studies in mice have confirmed the importance of dietary sugars in precipitating s…”
BackgroundInfluential
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Mechanisms of NAFLD development and therapeutic strategies
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The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology
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Liver Cancer: Connections with Obesity, Fatty Liver, and Cirrhosis
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Lipidomics for studying metabolism
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Mechanisms of Fibrosis Development in Nonalcoholic Steatohepatitis
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Impaired autophagic flux is associated with increased endoplasmic reticulum stress during the development of NAFLD
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Nonalcoholic Fatty Liver Disease: Pathogenesis and Disease Spectrum
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The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association
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Recent insights into the pathogenesis of nonalcoholic fatty liver disease
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Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation
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The Role of Cholesterol in the Pathogenesis of NASH
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Nonalcoholic Fatty Liver Disease and the Heart
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The lipogenic transcription factor ChREBP dissociates hepatic steatosis from insulin resistance in mice and humans
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Obesity and cancer: inflammation bridges the two
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The NLRP3 inflammasome: Mechanism of action, role in disease and therapies
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Molecular pathways in non-alcoholic fatty liver disease
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Targeted therapeutics and novel signaling pathways in non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH)
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Pathological Features of Fatty Liver Disease
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GS-0976 Reduces Hepatic Steatosis and Fibrosis Markers in Patients With Nonalcoholic Fatty Liver Disease
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Nontriglyceride Hepatic Lipotoxicity: The New Paradigm for the Pathogenesis of NASH
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Self-citation
Lipotoxicity as the Leading Cause of Non-Alcoholic Steatohepatitis
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Steatosis in the Liver
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Self-citation
New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis
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Authors: Neuschwander‐Tetri, B. A.
Affiliations: Saint Louis University (US)
Corresponding author: Neuschwander‐Tetri, Brent A.
ORCID: Neuschwander‐Tetri, Brent A.
Venue: Hepatology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2010-08
Volume: 52
Issue: 2
Pages: 774-788
ISSN: 0270-9139 (ISSN-L)
DOI: 10.1002/hep.23719
OpenAlex: W2107943478
Cited by: 1,077
References: 196
Citations by year: 2026: 29 · 2025: 61 · 2024: 66 · 2023: 78 · 2022: 75 · 2021: 86 · 2020: 106 · 2019: 72 · 2018: 66 · 2017: 72 · 2016: 77 · 2015: 60 · 2014: 64 · 2013: 52 · 2012: 47
FWCI: 5.87
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 1857 d)
Locations: Hepatology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Keywords: nonalcoholic steatohepatitis, hepatic lipotoxicity, NASH pathogenesis, triglyceride accumulation, insulin resistance, de novo lipogenesis, adipose tissue insulin sensitivity, lipolysis, carbohydrate intake, physical activity, muscle glucose uptake
MeSH terms: Fatty Acids, Fatty Liver, Humans, Insulin Resistance, Liver, Causality, Oxidative Stress, Lipid Metabolism

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Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites†

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