2014 Fiscal Year Final Research Report
Mifepristone improved Diet-induced insulin resistance by increasing blood level of adiponectin.
| Project/Area Number |
25860770
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Endocrinology
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Keywords | 前駆脂肪細胞 / 成熟脂肪細胞 / グルココルチコイド / デキサメタゾン / 脂肪細胞分化 / スフィンゴ脂質 / S1P / スフィンゴシンキナーゼ |
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| Outline of Final Research Achievements |
Mifepristone is known as a steroid receptor antagonist and is clinically used as an anti-cancer agent. This study aimed to determine whether mifepristone influences insulin sensitivity and adiponectin secretion both in in vivo and in vitro. First, we explored the effects of mifepristone, on metabolic functions in obese mice. When these mice were fed mifepristone, they exhibited a marked improvement in insulin sensitivity, and attenuated hepatic injury, compared with mice that received only the high-fat diet. Intriguingly, mifepristone-treated mice showed significantly elevated plasma adiponectin levels. Second, we tested the effects of mifepristone on differentiated adipocytes in vitro. When adipocytes were treated with mifepristone, adiponectin was upregulated at both mRNA and protein levels. These results uncover a possibility that long term administration of mifepristone leads to non-obese non-alcoholic fatty liver disease, associated with overeating or dyslipidemia.
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| Free Research Field |
生理学
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