Article Text

Download PDFPDF
When alcohol and fat meet, neutrophil traps form to promote liver injury
  1. Gavin E Arteel1,
  2. Bin Gao2
  1. 1 Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, Pittsburgh Liver Research Center, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
  2. 2 Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA
  1. Correspondence to Dr Bin Gao, Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA; bgao{at}mail.nih.gov; Dr Gavin E Arteel, Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, USA; gearteel{at}pitt.edu

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Steatotic liver diseases (SLDs) have a complicated history. Although it has been well recognised for centuries that obesity and alcohol consumption are associated with fatty liver and liver disease, acceptance that both are causal comorbities in SLD came much later. In the case of alcohol consumption, it was the work of Charles Lieber and colleagues that convincingly demonstrated that alcohol consumption, in lieu of other factors (eg, nutritional deficiencies) was sufficient to cause SLD. Similarly, the work of Ludwig and colleagues first clearly demonstrated that obesity can be directly causal in SLD in lieu of cryptogenic alcohol misuse. These findings led to the development of two clear and distinct SLDs, alcohol-related liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD).

Although studies defining ALD and NAFLD were seminal and paved the way for future research, the need to unequivocally prove the underlying causality between ALD and NAFLD led to some unintended consequences. Namely, both in human disease and in preclinical models, ALD and NAFLD tended to be studied in separate but parallel fields. The diagnosis of ALD and NAFLD generally had relatively strict cut-offs of daily alcohol consumption (ie, high for ALD, low for NAFLD). This siloing …

View Full Text

Footnotes

  • Contributors GEA: writing-original draft, writing-review and editing. BG: writing-review and editing.

  • Funding This study was funded by National Institute on Alcohol Abuse and Alcoholism (Intramural program, R01 AA021978)

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

Linked Articles