Obesity-induced inflammation and insulin resistance
Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic disorder such as type 2 diabetes, fatty liver disease and cardiovascular disease. Insulin resistance is an underlying...
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| Main Author: | |
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| Format: | Electronic Book Chapter |
| Language: | English |
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Frontiers Media SA
2014
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| Series: | Frontiers Research Topics
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| Subjects: | |
| Online Access: | DOAB: download the publication DOAB: description of the publication |
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| Summary: | Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic disorder such as type 2 diabetes, fatty liver disease and cardiovascular disease. Insulin resistance is an underlying basis for the pathogenesis of these metabolic diseases. Overnutrition or obesity activates the innate immune system with subsequent recruitment of immune cells such as macrophages and T cells, which contributes to the development of insulin resistance. In particular, 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). ATMs are a prominent source of proinflammatory cytokines, such as TNF-a 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. All articles in this topic highlight the interconnection between obesity, inflammation, and insulin resistance in all its diversity to the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of insulin resistance and diabetes. |
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| Physical Description: | 1 electronic resource (120 p.) |
| ISBN: | 978-2-88919-428-5 9782889194285 |
| Access: | Open Access |