2015 Fiscal Year Final Research Report
Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization
| Project/Area Number |
25461332
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Yahagi Naoya 筑波大学, 医学医療系, 准教授 (60420246)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 糖・脂質代謝 / 神経 / グリコーゲン |
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| Outline of Final Research Achievements |
During fasting, animals maintain their energy balance by shifting their energy source from carbohydrates to triglycerides. Here we show that a selective hepatic vagotomy slows the speed of fat consumption by attenuating sympathetic nerve-mediated lipolysis in adipose tissue. Hepatic glycogen pre-loading by the adenoviral overexpression of glycogen synthase or the transcription factor TFE3 abolished this liver-brain-adipose axis activation. Moreover, the blockade of glycogenolysis [corrected] through the knockdown of the glycogen phosphorylase gene and the resulting elevation in the glycogen content abolished the lipolytic signal from the liver, indicating that glycogen is the key to triggering this neurocircuitry. These results demonstrate that liver glycogen shortage activates a liver-brain-adipose neural axis that has an important role in switching the fuel source from glycogen to triglycerides under prolonged fasting conditions.
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| Free Research Field |
代謝学
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