2012 Fiscal Year Final Research Report
Effect of DPP-4 inhibitor on chronic adipose tissue inflammation in obesity mouse model
| Project/Area Number |
23650230
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KYUWA Shigeru 東京大学, 大学院・農学生命科学研究科, 教授 (30177943)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 疾患モデル / 糖尿病 / 慢性炎症 / 脂肪組織 / 免疫 / NKT 細胞 / インターフェロン-γ / 相互作用 |
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| Research Abstract |
To understand a physiological and pathological role of natural killer T (NKT) cells on inflammation in adipose tissue, we characterized a subset of NKT cells in abdominal and subcutaneous adipose tissues in C57BL/6J mice fed on normal or high-fat diets. NKT cells comprised a larger portion of lymphocytes in adipose tissues compared to the spleen and peripheral blood, Furthermore, some NKT cells in adipose tissues expressed higher levels of CD69 and intracellular interferon-γ. We speculate that the NKT cells in adipose tissues may form an equivalent subset in other tissues and that these subsets are likely to participate in adipose tissue inflammation. Additionally, the high expression level of CD69 and intracellular IFN-γ raises the possibility that some NKT cells in adipose tissue may be stimulated by some physiological mechanism. IFN-γ suppressed adipogenesis in 3T3-L1 preadipocytes. CD1d1 was expressed in 3T3-L1 mature adipocytes and was enhanced by IFN-γ stimulation. Cocultures of NKT cells and 3T3-L1 adipocytes resulted in increased IFN-γ secretion from NKT cells and increased CD1d1 expression in adipocytes in an IFN-γ-dependent manner. Our findings strongly suggest that iNKT cells communicate with adipocytes via CD1d1 and IFN-γ.
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