2013 Fiscal Year Final Research Report
Roles of glucocorticoid receptors in cardiac and adipose tissue pathology in a rat model of metabolic syndrome
Project/Area Number |
24590690
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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 |
Laboratory medicine
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Research Institution | Nagoya University |
Principal Investigator |
NAGATA Kohzo 名古屋大学, 医学(系)研究科(研究院), 教授 (20378227)
|
Co-Investigator(Renkei-kenkyūsha) |
UEYAMA Jun 名古屋大学, 医学系研究科, 准教授 (00397465)
HASHIMOTO Katsunori 名古屋大学, 医学系研究科, 助教 (70324423)
ITO Hiromi 名古屋大学, 医学系研究科, 助教 (20610752)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | メタボリックシンドローム / ストレス / グルココルチコイド受容体 / βアドレナリン受容体 / 心筋傷害 / 脂肪組織炎症 / 糖代謝異常 |
Research Abstract |
We first clarified the pathophysiological roles of the glucocorticoid-glucocorticoid receptor (GR) axis in cardiac and adipose tissue pathology of DahlS.Z-Leprfa/Leprfa (DS/obese) rats as a new animal model of metabolic syndrome (MetS). We next investigated the responses to cold stress and restraint stress in these rats. Cold stress and the GR blocker RU486 did not affect obesity in DS/obese rats. In contrast, restraint stress to DS/obese rats attenuated obesity in a manner sensitive to the beta-adrenergic receptor blocker propranolol. Both types of stress exacerbated hypertension, cardiac injury, adipose tissue inflammation, and glucose metabolism, and all of these effects were ameliorated by RU486 with cold stress and by propranolol with restraint stress.
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