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Cited by 2,089Liver Disease Diagnosis and TreatmentAlcohol Consumption and Health EffectsLiver physiology and pathology

Human Fatty Liver Disease: Old Questions and New Insights

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Cohen, Jonathan C., Horton, Jay D., Hobbs, Helen H.·2011·Science
DOI 10.1126/science.1204265PMC PMC3229276
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Abstract

Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem that affects one-third of adults and an increasing number of children in developed countries. The disease begins with the aberrant accumulation of triglyceride in the liver, which in some individuals elicits an inflammatory response that can progress to cirrhosis and liver cancer. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood, and therapeutic options are limited. Here, we discuss recent mechanistic insights into NAFLD, focusing primarily on those that have emerged from human genetic and metabolic studies.

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Crossref · 10.1126/science.1204265

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52 of 52 references verified0 citation errors · 0 not checkable

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  • Impairment in mitochondrial function and ATP generation is observed in NAFLD.

    “Impairment in mitochondrial function and ATP generation is also observed.”

    From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [7]

    In “What Factors Contribute to NAFLD Progression?” (page not provided), the paper says saturated fats can inhibit mitochondrial function in model organisms. It does not report impaired ATP generation or establish that mitochondrial impairment was observed in people with NAFLD. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Oxidative stress contributes to the production of reactive oxygen species, lipid peroxidation products and decreases the levels of antioxidants such as superoxide dismutase, glutathione, and catalase.

    “Oxidative stress contributes to the production of reactive oxygen species, lipid peroxidation products and decreases the levels of antioxidants such as superoxide dismutase, glutathione, and catalase.”

    From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [7]

    The section “What Factors Contribute to NAFLD Progression?” mentions oxidative-stress pathways as implicated in progression to NASH, but does not describe the effects attributed to oxidative stress here. Searches for reactive oxygen species, lipid peroxidation, superoxide dismutase, glutathione, and catalase found no passage establishing their production or decreased levels. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

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Cites

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1 of the 53 references couldn’t be matched to a known paper.

Research works printed but not linked: 49

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Authors
Cohen, J. C., Horton, J. D., & Hobbs, H. H.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Howard Hughes Medical Institute (US)
Corresponding author
Hobbs, Helen H.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2011-06-24
Volume
332
Issue
6037
Pages
1519-1523
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.1204265
PMC
PMC3229276
OpenAlex
W2065612971
Cited by
2,089
References
53
Citations by year
2026: 38 · 2025: 88 · 2024: 103 · 2023: 118 · 2022: 139 · 2021: 152 · 2020: 168 · 2019: 158 · 2018: 166 · 2017: 170 · 2016: 153 · 2015: 171 · 2014: 143 · 2013: 171 · 2012: 122
FWCI
17.33
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (P01 HL-20948, P01HL020948, RL1HL092550)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK090066)
  • National Institute of Dental and Craniofacial Research (UL1DE019584, UL1DE109584)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
non-alcoholic fatty liver disease, hepatic triglyceride accumulation, liver inflammation, liver cirrhosis, hepatocellular carcinoma, obesity, insulin resistance, NAFLD pathogenesis, genetic susceptibility, metabolic mechanisms
MeSH terms
Animals, Dietary Fats, Disease Models, Animal, Fatty Liver, Female, Humans, Insulin Resistance, Liver, Liver Cirrhosis, Liver Neoplasms, Male, Obesity, Triglycerides, Disease Progression, Genetic Predisposition to Disease, Non-alcoholic Fatty Liver Disease

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