2013 Fiscal Year Final Research Report
Identification of the molecular mechanisms in between adipose tissue dysfunction and metabolic syndrome
| Project/Area Number |
24790740
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | 脂肪組織機能異常 / 慢性炎症 / 肥満症 / メタボリックシンドローム |
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| Research Abstract |
Obesity has become a global health and social burden. Obesity is known to induce inflammation within visceral adipose tissue, which contributes to the development of metabolic and cardiovascular disease. However, it remains unknown how adipose inflammation is initiated. In obesity, adipose tissue expands through both the hypertrophy and hyperplasia of adipocytes. We found that during adipocyte hyperplasia, adipocyte progenitors give rise to two cell populations: adipocytes and CD34+CD29+Sca-1intCD24+ adipocyte progenitor-derived proinflammatory (APDP) cells. While APDP cells appear to support angiogenesis that is tightly linked to adipogenesis, their transplantation into lean adipose tissue induced inflammation and systemic insulin resistance partly by producing proinflammatory cytokines and recruiting monocytes. Our results demonstrate that adipocyte hyperplasia triggers an inflammatory cascade through generation of APDP cells.
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Research Products
(15 results)
