| Project/Area Number |
16H06668
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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 | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
|
| 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 | 肥満 / 脂肪組織 / 核内受容体 / 転写因子 / PPARg / エピジェネティック / 糖尿病 / PPARｇ |
|---|
| Outline of Final Research Achievements |
HELZ2 KO mice show the resistance for obesity and fatty liver. However, the function of HELZ 2 in adipose tissue (white adipose tissue, brown adipose tissue) is unknown, and functional analysis of HELZ2 in metabolic tissues was carried out in vivo.
In adipose tissue, the effect of the Pioglitazone was attenuated in KO mice. In addition, the expression levels of PPARg target genes ware not increased in Ko mice. In the acute cold exposure test, the body temperature was not decreased in KO mice compared with WT at acute cold exposure. In the mouse liver, it was confirmed that expression level of Helz2 gene was increased in the light phase period. In WAT, expression changes other than the light and dark periods were observed.
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