4.3 Review

Molecular mechanism of obesity-induced metabolic' tissue remodeling

Journal

JOURNAL OF DIABETES INVESTIGATION
Volume 9, Issue 2, Pages 256-261

Publisher

WILEY
DOI: 10.1111/jdi.12769

Keywords

Chronic inflammation; Obesity; Macrophages

Funding

  1. Ministry of Education, Culture, Sports, Science and Technology of Japan [16H05171, 16KT0110, 16K08732, 17K19686, 17H05500]
  2. Japan Agency for Medical Research and Development (CREST)
  3. Takeda Science Foundation
  4. Takeda Medical Research Foundation
  5. Medical Research Institute
  6. Tokyo Medical and Dental University
  7. Grants-in-Aid for Scientific Research [16KT0110, 16K08732, 17H05500, 16K15234, 17K19686, 15K09423, 16H05171] Funding Source: KAKEN

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Chronic inflammation is a common molecular basis underlying a variety of chronic diseases. Accumulating evidence has also suggested that chronic inflammation contributes to the pathogenesis of obesity and diabetes, which have been considered as metabolic diseases. For the past several decades, there has been dramatic progress in understanding the underlying mechanism of adipose tissue dysfunction induced by obesity. Tissue remodeling is one of the histological features of chronic inflammation, in which stromal cells dramatically change in number and cell type. Indeed, adipose tissue remodeling is induced by various stromal cells, and results in the impairment of adipose tissue function, such as adipocytokine production and lipid storage, which leads to systemic metabolic disorder. In addition to adipose tissue, the liver is another example of obesity-induced tissue remodeling. In the present review, we discuss how obesity induces interstitial fibrosis in adipose tissue and the liver, particularly focusing on the role of macrophages.

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