Study for the interaction between skeletal muscle and the liver on the regulation of metabolic control via the transcription factor KLF15
| Project/Area Number |
16H06970
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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 | Kobe University |
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Principal Investigator |
Okada Yuko 神戸大学, 医学部附属病院, 助教 (90782433)
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| Co-Investigator(Renkei-kenkyūsha) |
OGAWA Wataru 神戸大学, 大宇学院医学研究科, 教授 (40294219)
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| Research Collaborator |
HIRATA Yu 大学院
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | エネルギー代謝骨 / 骨格筋 / 糖尿病 / エネルギー代謝 |
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| Outline of Final Research Achievements |
We have investigated the role of the transcription factor KLF15 in the regulation of systemic metabolism. The abundance of KLF15 in skeletal muscle is upregulated in response to exercise, which is likely mediated via calcium-dependent signaling. The abundance of KLF15 in skeletal muscle is also upregulated in several diabetic model mice and treatment of cultured muscle cells with a high concentration of glucose resulted in the increase in the protein abundance of the transcription factor. Hyperglycemia-induced increase in the protein abundance of KLF15 is attributable to the decrease in the poly-ubiquitination of this protein. Whereas blood glucose levels of muscle-specific KLF15 deficient mice are similar to those of control mice, those of the mutant mice at fasting states are lower, suggesting that KLF15 in skeletal muscle contribute to the regulation of hepatic gluconeogenesis.
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Report
(3 results)
Research Products
(6 results)
