2004 Fiscal Year Final Research Report Summary
Clarification of the molecular mechanism(s) behind exercise training-induced suppression of fat mass
| Project/Area Number |
15300222
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | Tokyo Metropolitan University |
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Principal Investigator |
IZAWA Tetsuya Tokyo Metropolitan University, Graduate School of Science, Professor, 理学研究科, 教授 (70147495)
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| Project Period (FY) |
2003 – 2004
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| Keywords | exercise / lipogenic gene / TNF-α / apoptosis / diet / adipocyte / fat mass / rat |
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| Research Abstract |
In order to clarify the mechanism(s) behind either exercise- or exercise training-induced suppression of fat mass, the following studies were performed in rat adipocytes : (1)effects of exercise on apoptotic and anti-apoptotic signals, (2)effects of exercise and diet on several genes related with lipid metabolism, (3)effects of exercise on tumor necrosis factor-α (TNF-α)-induced apoptotic and anti-apoptotic signals, (4)effect of exercise training on insulin secretion from pancreatic islets, (5)alterations in exercise-induced β-adrenergic receptors and G proteins. As a result, the following findings were obtained. Exercise increased the Bcl2/Bax ratio in retroperitoneal and inguinal adipose tissue, but decreased its ratio in epididymal adipose tissue. Starvation reduced the expressions of some lipogenic genes, and re-feeding enhanced these expressions. Exercise after re-feeding blocked re-feeding-induced enhancement of some lipogenic genes expressions. Exercise training enhanced TNF-α signaling directed toward the expressions of survival signals and the suppression of fatty acid synthase gene expression. The mechanism behind exercise training-induced reduction of insulin secretion may involve an enhanced expression of neuronal nitric oxide synthase and a decreased expression of Gαi-2 protein. Acute exercise altered the expression of Giα2 protein via the ubiquitin-proteasome pathway, and the mechanism underlying the increased density of β_2-AR after exercise may involve alterations in a multi-step event involving the coordinate interaction among proteins mediating β_2-AR trafficking, e.g. G-protein-coupled receptor kinase-2 and β-arrestin-2. Thus, the data obtained in this grant will become helpful to understand more exact mechanism behind exercise training-induced suppression of fat mass.
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Research Products
(10 results)
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[Journal Article] β-Adrenergic receptor trafficking by exercise in rat adipocytes : Roles of G-protein-coupled receptor kinase-2, β-arrestin-2, and the ubiquitin-proteasome pathway.2006
Author(s)
Ogasawar, J., Sanpei M., Rahman N., Sakurai T., Kizaki T., Hitomi Y., Ohno H., Izawa T.
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Journal Title
Description
「研究成果報告書概要(和文)」より
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[Journal Article] Exercise Training Enhances Tumor Necrosis Factor-□-Induced Expressions of Anti-Apoptotic Genes without Alterations in Caspase-3 Activity in Rat Epididymal Adipocytes. 20052005
Author(s)
Sakurai T, Takei M, Ogasawara J, Watanabe N, Sanpei M, Yoshida M, Nakae D, sakurai T, Nakano N, Kizaki T, Ohno H, Izawa T.
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Journal Title
Jan J Physiol 53・5(in press)
Description
「研究成果報告書概要(和文)」より
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[Journal Article] 「研究成果報告書概要(欧文)」より2005
Author(s)
Sakurai T, Takei M, Ogasawara J, Watanabe N, Sanpei M, Yoshida M, Nakae D, Sakurai T, Nakano N, Kizaki T, Ohno H, Izawa T.
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Journal Title
Jpn J Physiol 53(5)(in press)
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