The mechanisms by which protein malnutrition increases circulating adiponectin levels in rats
Project/Area Number |
25850095
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Food science
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Research Institution | Nippon Medical School |
Principal Investigator |
Toyoshima Yuka 日本医科大学, 付置研究所, 講師 (70516070)
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Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | アディポネクチン / 低タンパク質栄養 / 脂肪細胞 / 低タンパク質食 / インスリン / インスリン様成長因子 / タンパク質栄養 / エネルギー消費 / インスリンシグナル / 耐糖能 / アミノ酸 |
Outline of Final Research Achievements |
Adiponectin is a protein that is mainly secreted from adipocytes and exhibits an antidiabetic property, which enhances insulin action. Our previous studies showed that protein malnutrition caused increases in circulating adiponectin levels in growing rats. In this study, we found that the enhancement of adiponectin secretion from adipocytes and/or the suppression of its degradation in the blood result in the elevation of circulating adiponectin levels in protein-malnourished rats. Furthermore, it was suggested that lower circulating insulin and insulin-like growth factor-1 contribute to enhance adiponectin secretion from adipocytes under protein malnutrition.
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Report
(4 results)
Research Products
(8 results)
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[Journal Article] Tissue-specific effects of protein malnutrition on insulin signaling pathway and lipid accumulation in growing rats2014
Author(s)
Yuka Toyoshima, Reiko Tokita, Yusuke Taguchi, Narumi Akiyama-Akanishi, Asako Takenaka, Hisanori Kato, Kazuhiro Chida, Fumihiko Hakuno, Shiro Minami, Shin-Ichiro Takahashi
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Journal Title
Endocrine Journal
Volume: 61
Issue: 5
Pages: 499-512
DOI
NAID
ISSN
0918-8959, 1348-4540
Related Report
Peer Reviewed
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