2014 Fiscal Year Final Research Report
Dietary zinc-deficiency-induced changes in the expressions of adrenaline receptors and mitochondrial uncoupling protein (UCP)-1, and immuno-responsive functions in rats
| Project/Area Number |
24300261
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Eating habits, studies on eating habits
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| Research Institution | Waseda University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
白土 健 杏林大学, 医学部, 助教 (60559384)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 亜鉛（Zn）欠乏 / インスリン様成長因子‐１（IGF-1） / IGF-1受容体 （IGF-1R) / アドレナリン受容体 (AR) / 褐色脂肪組織 (BAT) / グルココルチコイド受容体 （GR) / 脱共役タンパク質（UCP)-1～３ / ラット骨格筋 |
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| Outline of Final Research Achievements |
The effects of zinc(Zn)-deficiency on the expression of insulin-like growth factor-1（IGF-1)receptor(IGF-1R) in skeletal muscles of weaned SD male rats were studied. After the experiment for 2 and 4 weeks, the slow-twitch soleus (SOL) and fast-twitch extensor digitorum longus (EDL) muscles were isolated. Zn-deficiency for 4 weeks caused a significant reduction in the EDL of muscles. However, that of SOL muscles was not chnaged by Zn-deficiency. IGF1-R mRNA expression in EDL muscles significantly increased by 1.3 times in 2 and 4 weeks, whereas significant changes were not observed in SOL muscles. By contrast, IGF-1R protein expression in SOL muscles significantly increased by 2.1 times in 4 weeks, although significant changes were not observed in EDL muscles. These results suggest that the incresed expression of IGF-1R protein in SOL muscles in response to Zn-deficiency play an important role in the attenuation of delayed muscle development due to reduced plasma IGF-1 concentrations.
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| Free Research Field |
総合領域・生活科学
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