2013 Fiscal Year Final Research Report
Analysis of function of glucocorticoid receptor expressed in NPY neurons
| Project/Area Number |
23591350
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
ARIMA Hiroshi 名古屋大学, 医学(系)研究科(研究院), 准教授 (50422770)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OISO Yutaka 名古屋大学, 大学院医学系研究科, 教授 (40203707)
BANNO Ryoichi 名古屋大学, 医学部附属病院, 助教 (80597865)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Keywords | グルココルチコイドレセプター / 視床下部 / 肥満 |
|---|
| Research Abstract |
Body weight and white adipose tissues weight were significantly less in AgRP neuron-specific knockout of glucocorticoid receptor mice compared to wild-type mice when they were subjected to a high fat diet. The expression levels of UCP1 mRNA in the brown adipose tissues were significantly higher in the knockout mice than in wild-type mice. On the other hand, thapsigargin, an ER stressor, increased phosphorylation of p65 and attenuated expression of AgRP and NPY mRNA stimulated by dexamethasone in hypothalamic cultures of wild-type mice. Furthermore, it is demonstrated that inhibitor of p65 cancelled the effects of thapsigargin on the AgRP and NPY mRNA expression stimulated by dexamethasone.
|
