Project/Area Number |
20790660
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Endocrinology
|
Research Institution | Kyoto University |
Principal Investigator |
PARK Kwijun Kyoto University, 医学研究科, 非常勤講師 (20437221)
|
Research Collaborator |
TAMURA Naohsa 京都大学, 医学研究科, 講師 (40314207)
SONOYAMA Takuhiro 京都大学, 医学研究科, 大学院生
|
Project Period (FY) |
2008 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | ナトリウム利尿ペプチド / 末梢動脈疾患 / 受容体 / 遺伝子発現 / 治療法 |
Research Abstract |
We tried to investigate the influence of diabetic status on the expression of natriuretic peptide receptors (NPRs) in the peripheral artery, but it was suggested that investigations using larger animals such as rats would be needed to address this issue. It was suggested that atrial natriuretic peptide (ANP) administration at a high dose in mice would result in the activation of sympathetic nervous system in response to the blood pressure decrease by ANP. In the skeletal muscle in mice with the high-fat diet-induced obesity and impaired glucose tolerance, mRNA expression of guanylyl cyclase (GC)-A, the signaling receptor for ANP and brain natriuretic peptide, was decreased and that of NPR-C, the clearance receptor for NPs, was increased as compared with mice fed normal chaw, indicating that obesity and impaired glucose tolerance would suppress the signaling of NP system.
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