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International Journal of Cell Biology
Volume 2014, Article ID 519153, 9 pages
Review Article

An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease

1Division of Cardiovascular and Metabolic Diseases, Institut de Recherches Cliniques de Montreal 110, Avenue des Pins Ouest, Montreal, QC, Canada H2W 1R7
2Molecular Biology Department, University of Montreal, Montreal, QC, Canada H3C 3J7

Received 20 June 2013; Accepted 20 December 2013; Published 12 February 2014

Academic Editor: Julie St-Pierre

Copyright © 2014 Aurèle Besse-Patin and Jennifer L. Estall. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress damages multiple cellular components including DNA, lipids, and proteins and has been linked to pathological alterations in nonalcoholic fatty liver disease (NAFLD). Reactive oxygen species (ROS) emission, resulting from nutrient overload and mitochondrial dysfunction, is thought to be a principal mediator in NAFLD progression, particularly toward the development of hepatic insulin resistance. In the context of insulin signalling, ROS has a dual role, as both a facilitator and inhibitor of the insulin signalling cascade. ROS mediate these effects through redox modifications of cysteine residues affecting phosphatase enzyme activity, stress-sensitive kinases, and metabolic sensors. This review highlights the intricate relationship between redox-sensitive proteins and insulin signalling in the context of fatty liver disease, and to a larger extent, the importance of reactive oxygen species as primary signalling molecules in metabolically active cells.