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An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver
Aurèle Besse-Patin1, Jennifer L Estall1
1Division of Cardiovascular and Metabolic Diseases, Institut de Recherches Cliniques de Montreal 110, Avenue des Pins Ouest, Montreal, QC, Canada H2W 1R7 ; Molecular Biology Department, University of Montreal, Montreal, QC, Canada H3C 3J7.
Abstract:
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.
Insights
Oxidative stress and reactive oxygen species (ROS) play a key role in nonalcoholic fatty liver disease (NAFLD) progression and insulin resistance. Understanding ROS signaling is crucial for managing fatty liver disease.
Area of Science:
- Biochemistry
- Cell Biology
- Hepatology
Background:
- Oxidative stress damages cellular components like DNA, lipids, and proteins.
- Nonalcoholic fatty liver disease (NAFLD) is associated with oxidative stress and reactive oxygen species (ROS) production.
- ROS are implicated in NAFLD progression and the development of hepatic insulin resistance.
Purpose of the Study:
- To review the complex interplay between redox-sensitive proteins and insulin signaling in NAFLD.
- To emphasize the role of ROS as signaling molecules in metabolically active cells within the context of fatty liver disease.
Main Methods:
- Literature review focusing on oxidative stress, ROS, and insulin signaling pathways.
- Analysis of studies investigating redox modifications of proteins involved in metabolic regulation.
- Synthesis of current understanding of ROS dual role in insulin signaling.
Main Results:
- ROS emission, driven by nutrient overload and mitochondrial dysfunction, is a primary driver of NAFLD.
- ROS exhibit a dual role in insulin signaling, acting as both facilitators and inhibitors.
- Redox modifications of cysteine residues by ROS impact enzyme activity, kinases, and metabolic sensors.
Conclusions:
- The relationship between redox-sensitive proteins and insulin signaling is intricate in NAFLD.
- ROS are critical signaling molecules in metabolically active cells, influencing NAFLD pathogenesis.
- Targeting ROS pathways may offer therapeutic strategies for NAFLD and associated insulin resistance.
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