Adipose Tissue Remodeling as Homeostatic Inflammation
Evidence has accumulated indicating that obesity is associated with a state of chronic, low-grade inflammation. Obese adipose tissue is characterized by dynamic changes in cellular composition and function, which may be referred to as “adipose tissue remodeling”. Among stromal cells in the adipose t...
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Wiley
2011-01-01
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Series: | International Journal of Inflammation |
Online Access: | http://dx.doi.org/10.4061/2011/720926 |
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author | Michiko Itoh Takayoshi Suganami Rumi Hachiya Yoshihiro Ogawa |
author_facet | Michiko Itoh Takayoshi Suganami Rumi Hachiya Yoshihiro Ogawa |
author_sort | Michiko Itoh |
collection | DOAJ |
description | Evidence has accumulated indicating that obesity is associated with a state of chronic, low-grade inflammation. Obese adipose tissue is characterized by dynamic changes in cellular composition and function, which may be referred to as “adipose tissue remodeling”. Among stromal cells in the adipose tissue, infiltrated macrophages play an important role in adipose tissue inflammation and systemic insulin resistance. We have demonstrated that a paracrine loop involving saturated fatty acids and tumor necrosis factor-α derived from adipocytes and macrophages, respectively, aggravates obesity-induced adipose tissue inflammation. Notably, saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 complex, thereby activating macrophages. Such a sustained interaction between endogenous ligands derived from parenchymal cells and pathogen sensors expressed in stromal immune cells should lead to chronic inflammatory responses ranging from the basal homeostatic state to diseased tissue remodeling, which may be referred to as “homeostatic inflammation”. We, therefore, postulate that adipose tissue remodeling may represent a prototypic example of homeostatic inflammation. Understanding the molecular mechanism underlying homeostatic inflammation may lead to the identification of novel therapeutic strategies to prevent or treat obesity-related complications. |
format | Article |
id | doaj-art-465dbbe9cf5547c1a35aa2e5f3c2d98a |
institution | Kabale University |
issn | 2042-0099 |
language | English |
publishDate | 2011-01-01 |
publisher | Wiley |
record_format | Article |
series | International Journal of Inflammation |
spelling | doaj-art-465dbbe9cf5547c1a35aa2e5f3c2d98a2025-02-03T01:21:56ZengWileyInternational Journal of Inflammation2042-00992011-01-01201110.4061/2011/720926720926Adipose Tissue Remodeling as Homeostatic InflammationMichiko Itoh0Takayoshi Suganami1Rumi Hachiya2Yoshihiro Ogawa3Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, JapanDepartment of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, JapanDepartment of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, JapanDepartment of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, JapanEvidence has accumulated indicating that obesity is associated with a state of chronic, low-grade inflammation. Obese adipose tissue is characterized by dynamic changes in cellular composition and function, which may be referred to as “adipose tissue remodeling”. Among stromal cells in the adipose tissue, infiltrated macrophages play an important role in adipose tissue inflammation and systemic insulin resistance. We have demonstrated that a paracrine loop involving saturated fatty acids and tumor necrosis factor-α derived from adipocytes and macrophages, respectively, aggravates obesity-induced adipose tissue inflammation. Notably, saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 complex, thereby activating macrophages. Such a sustained interaction between endogenous ligands derived from parenchymal cells and pathogen sensors expressed in stromal immune cells should lead to chronic inflammatory responses ranging from the basal homeostatic state to diseased tissue remodeling, which may be referred to as “homeostatic inflammation”. We, therefore, postulate that adipose tissue remodeling may represent a prototypic example of homeostatic inflammation. Understanding the molecular mechanism underlying homeostatic inflammation may lead to the identification of novel therapeutic strategies to prevent or treat obesity-related complications.http://dx.doi.org/10.4061/2011/720926 |
spellingShingle | Michiko Itoh Takayoshi Suganami Rumi Hachiya Yoshihiro Ogawa Adipose Tissue Remodeling as Homeostatic Inflammation International Journal of Inflammation |
title | Adipose Tissue Remodeling as Homeostatic Inflammation |
title_full | Adipose Tissue Remodeling as Homeostatic Inflammation |
title_fullStr | Adipose Tissue Remodeling as Homeostatic Inflammation |
title_full_unstemmed | Adipose Tissue Remodeling as Homeostatic Inflammation |
title_short | Adipose Tissue Remodeling as Homeostatic Inflammation |
title_sort | adipose tissue remodeling as homeostatic inflammation |
url | http://dx.doi.org/10.4061/2011/720926 |
work_keys_str_mv | AT michikoitoh adiposetissueremodelingashomeostaticinflammation AT takayoshisuganami adiposetissueremodelingashomeostaticinflammation AT rumihachiya adiposetissueremodelingashomeostaticinflammation AT yoshihiroogawa adiposetissueremodelingashomeostaticinflammation |