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Signalling Networks Governing Metabolic Inflammation.
Nassim Dali-Youcef1,2, Romeo Ricci3,4
1Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC)/CNRS UMR 7104 - Inserm U 964/Université de Strasbourg, 1 rue Laurent Fries, 67404, Illkirch, France. dali@igbmc.fr.
Handbook of Experimental Pharmacology
|April 24, 2015
Summary
Low-grade inflammation, driven by overnutrition, promotes obesity and insulin resistance. Cellular stress and inflammatory pathways disrupt insulin signaling, contributing to type 2 diabetes development.
Area of Science:
- Metabolic inflammation
- Cellular signaling pathways
- Endocrinology
Background:
- Low-grade inflammation is a key factor in obesity, insulin resistance, and type 2 diabetes.
- Metabolic inflammation involves complex signaling events triggered by overnutrition, inflammatory cytokines, and lipid species.
Purpose of the Study:
- To summarize current knowledge on cellular signaling events impacting metabolic inflammation and whole-body metabolism.
- To highlight the interplay between signaling pathways in low-grade inflammation and insulin resistance.
Main Methods:
- Review of current scientific literature on metabolic inflammation signaling.
- Analysis of cellular stress responses including unfolded protein response and reactive oxygen species.
- Examination of inflammasome activation and canonical inflammatory pathways.
Main Results:
- Overnutrition induces inflammatory pathways via cytokines, lipids, inflammasomes, and cellular stress.
- Unfolded protein response and reactive oxygen species contribute to metabolic inflammation.
- Interplay between signaling pathways leads to insulin receptor pathway inactivation.
Conclusions:
- Cellular signaling events are critical mediators of metabolic inflammation.
- Disruption of insulin signaling by low-grade inflammation is a primary driver of insulin resistance and type 2 diabetes.
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