The mechanisms of anti-inflammatory effects by the activation of heat shock response

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591336
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Kumamoto University
• Principal Investigator: KONDO Tatsuya 熊本大学, 大学院生命科学研究部, 助教 (70398204)
• Co-Investigator(Kenkyū-buntansha): EIICHI Araki 熊本大学, 大学院生命科学研究部, 教授 (10253733)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 糖尿病 / 熱ショック応答経路 / HSP72 / AMPK

Outline of Final Research Achievements

Stimulation of several cell types with high glucose etc. increased ER stress and inflammatory signals, and these were attenuated by MET treatment. HSP72 siRNA with MET partially decreased this attenuation.
Obese diabetic model mice were treated with or without MET for 12 weeks. BW was not altered, but visceral adiposity was particularly decreased and glucose homeostasis, insulin resistance and chronic inflammation were improved. ER stress, oxidative stress and inflammatory signals were attenuated in liver and adipose tissues. When AMPK was knockdown, this amelioration was declined. These data support that MET activates not only HSP72 expression but also AMPK phosphorylation.

Free Research Field

糖尿病