2015 Fiscal Year Final Research Report
Metabolome study on mechanism of canine diabetes onset
Project/Area Number |
25450455
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Veterinary medical science
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Research Institution | Nippon Veterinary and Life Science University |
Principal Investigator |
Tazaki Hiroyuki 日本獣医生命科学大学, 獣医学部, 教授 (80231405)
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Co-Investigator(Kenkyū-buntansha) |
SATO Touko 日本獣医生命科学大学, 獣医学部, 助教 (70633478)
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Co-Investigator(Renkei-kenkyūsha) |
SAKO Toshinori 日本獣医生命科学大学, 獣医学部, 教授 (70153971)
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Research Collaborator |
NOZAWA Satoshi
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 糖尿病 / 副腎皮質機能亢進症 / 肥満 / メタボローム解析 / BCAA / TNF-α / 犬 |
Outline of Final Research Achievements |
The aim of this study was to analyse the characteristic metabolites of the diabetes onset in the dog and compare the difference between the hyperadrenocorticism (HAC) of the dog which reported in that diabetes develops following insulin resistance and the obesity of the dog. In canine myotube-like cell which added dexamethasone, glucose uptake ability was inhibited, and a catabolic reaction of the glucose tended to decrease.On the other hand, with canine myotube-like cells which added TNF-α, β-amino-isobutyric acid reinforcing insulin sensitivity significantly increase, and it is thought that it is action to compensate insulin resistance. Difference of these metabolites between HAC and obesity shows the cause that the HAC of the dogs leads to the diabetes onset, and the cause that the obesity of the dogs does not lead to diabetes. Thus, these results may be useful for further study of the diabetes onset mechanism in dogs.
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Free Research Field |
農学
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