| Project/Area Number |
26893335
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | Kansai Medical University (2015)
Department of Clinical Research, National Hospital Organization Kyoto Medical Center (2014) |
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Principal Investigator |
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | タンパク質 / レドックス / 炎症 / アディポサイトカイン / 小胞体 / 分泌 |
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| Outline of Final Research Achievements |
Accumulating evidence suggests a causal role played by adipose-derived secretory factors, adipocytokines, in the pathogenesis of obesity-related metabolic diseases. We aimed to determine the potential implications of endoplasmic reticulum (ER)-resident folding catalysts in the regulation of adipocytokine secretion. A series of redox enzymes were up-regulated during adipocyte differentiation, suggesting their involvement in adipocytokine synthesis and maturation in the ER. We also found that excessive fat accumulation and lipid peroxidation could induce the expression of thrombospondin 1 (THBS1), a potential mediator of tissue inflammation associated with obesity. Serum THBS1 levels showed a significant correlation with multiple traits of obesity/diabetes in Japanese subjects, particularly in women. THBS1 may act as a critical circulating factor that couples obesity with metabolic syndrome and diabetes in humans.
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