About this Research Topic
Obesity-induced chronic inflammation is crucial in the pathogenesis of insulin resistance, type 2 diabetes, and the metabolic syndrome. Obesity-associated systemic inflammation is characterized by increased circulating concentrations of proinflammatory cytokines and chemokines, and activation of pathways that regulate inflammation, including JNK and IKKβ/NF-κB pathways. A significant advance in our understanding of obesity-associated inflammation and insulin resistance has been recognition of the critical role of adipose tissue macrophages (ATMs) in both mice and humans. ATMs are a prominent source of proinflammatory cytokines, such as TNF-α and IL-6, that can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signaling and cause systemic insulin resistance via endocrine signaling, providing a potential link between inflammation and insulin resistance. Although the initiating factors of this inflammatory response remains to be fully determined, accumulating evidence supports that obesity-induced inflammation is mainly mediated by immune cells.
Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic diseases such as type 2 diabetes and cardiovascular disease. However, the links between nutrient sensing systems and the interface of metabolic and inflammatory responses are complex. Particularly, it is not clear how obesity or nutrient excess first regulates subsets of immune cells in circulation and induces local inflammation, including the recruitment and activation of ATMs. Furthermore, it is not determined in which cells or tissues inflammation initially occurs upon obesity, which then causes systemic inflammation and subsequent development of insulin resistance.
The Research Topic is to highlight the interconnection between obesity, inflammation, and insulin resistance. We encourage interested scientists to submit mini-reviews, methods papers, review articles, perspectives, and original research articles covering this topic in all its diversity to appreciate the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of obesity and diabetes.
Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic diseases such as type 2 diabetes and cardiovascular disease. However, the links between nutrient sensing systems and the interface of metabolic and inflammatory responses are complex. Particularly, it is not clear how obesity or nutrient excess first regulates subsets of immune cells in circulation and induces local inflammation, including the recruitment and activation of ATMs. Furthermore, it is not determined in which cells or tissues inflammation initially occurs upon obesity, which then causes systemic inflammation and subsequent development of insulin resistance.
The Research Topic is to highlight the interconnection between obesity, inflammation, and insulin resistance. We encourage interested scientists to submit mini-reviews, methods papers, review articles, perspectives, and original research articles covering this topic in all its diversity to appreciate the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of obesity and diabetes.
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