| Project/Area Number |
24790133
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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 |
Environmental pharmacy
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | メタロチオネイン / インスリンシグナル伝達 / 加齢性疾患 / 老化・寿命 / インスリンシグナル / インスリン |
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| Research Abstract |
In this study, we investigated involvement of metallothionein (MT) in insulin signaling pathways responsible for aging-related diseases. We showed that MT gene knockout mice (MTKO mice) had shorter lifespans than wild-type mice. MTKO mice had larger amounts of adipose tissues than wild type mice, and glucose metabolic capacity was greater in MTKO mice fed a high-fat diet than in the corresponding wild-type mice. Gene expression levels of adipocyte enlargement factor, Mest and lipoprotein receptor, Vldlr in adipose tissues were higher in MTKO mice than in wild type mice. We characterized gene and protein expression patterns of MT in adipogenesis model in vitro, 3T3-L1 cell line. In addition, pretreatment of MT siRNA promoted adipocyte differentiation in 3T3-L1 preadipocytes. MT knockout increased insulin-stimulated phosphorylation of Akt in mouse fibroblasts. Taken together, MT may protect against aging-related diseases through negative regulation of insulin signaling pathways.
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