2001 Fiscal Year Final Research Report Summary
Study on the associated regulation of energy and metabolism of glucose and lipids
| Project/Area Number |
10470235
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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 |
Metabolomics
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| Research Institution | Research Institute for Production Development |
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Principal Investigator |
INOUE Gen Research Institute for Production Development, Laboratory for Adult Diseases, Researcher, 成人病科学・研究室, 研究員 (20260606)
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| Co-Investigator(Kenkyū-buntansha) |
HOSODA Kiminori Kyoto University, Department of Life Science, Assistant professor, 人間環境学研究科, 助手 (40271598)
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| Project Period (FY) |
1998 – 1999
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| Keywords | energy metabolism / leptin / insulin / transgenic mouse / UCP3 / insulin sensitivity |
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| Research Abstract |
1.Using leptin-overexpressing transgenic mice and KKA^γ mice, we examined the effects of leptin on the development of obesity and diabetes. Leptin overexpressing KKA^γ mice became obese as KKA-γ mice did, while the development of diabetes in leptin overexpressing KKA^γ mice was significantly delayed compared to KKA^γ mice. The result suggests that leptin may be useful for the prevention of diabetes.
2.We found that insulin stimulated IRS1-associated PI3 kinase activity was increased in liver and skeletal muscles of leptin transgenic mice and themice intra cranially injectedwithieptin. However, could not find changes in Akt activity or the expression of constituents of intracellular insulin signal in liver and skeletal muscles of leptin transgenic mice. The results imply the divergent effects of leptin on insulin signaling system.
3.We already developed transgenic mice expressing UCP3 in skeletal muscles, and are going to explore the roles of energy expenditure on the regulation of glucose and lipid metabolism.
Ninna-ji Temple was founded in 888 AD. by the Emperor Uda at the request of his father, the former Emperor Kk, in the northwestern suburbs of the Capital-City Heian. Ninna-ji Temple hierarchically occupied the highest position among the, nonzeki temples whose abbots were members of the Impenal Family until the end of the Edo era, therefore the research of the documents which have been preserved at Ninna-ji Temple for centuries (the Ninna-ji Documents in general) contributes not only to the historical study of the temple, but also to the study of Japanese history.
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[Publications] T. Tanaka, H. Itoh, K. Doi, Y. Fukunaga, K. Hosotda, M. Shintani, J. Yamashita, T.H. Chun, M. Inoue, K. Masatsugu, N. Sawada, T. Saito, G. Inoue, H. Nishimura, Y. Yoshimasa, K. Nakao.: "Down regulation of peroxisome proliferator-activated receptor gamma expression by inflammatory cytokines and its reversal by thizaolidinediones."Diabetologia. 42 ; 6. 702-710 (1999)
Description
「研究成果報告書概要(欧文)」より
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[Publications] H. Masuzaki, Y. Ogawa, M. Aizawa-Abe, K. Hosoda, J. Suga, K. Ebihara, N. Satoh, H. Iwai, G. Inouse, H. Nishimura, Y. Yoshimasa, K. Nakao.: "Glucose metabolism and insulin sensitivity in transgenic mice overexpressing leption with lethal yellow agouti mutation : usefulness of leptin for the treatment of obsity-associated diabetes."Diabetes. 48:8. 1615-1622 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Y. Ogaw, H. Masuzaki, K. Hosoda, M. Aizawa-Abe, J. Suga, M. Suda, K. Ebihara, H. Iwai, N. Matsuoka, N. Satoh, H. Odaka, H.Kasuga, Y. Fujisawa, G. Inoue, H. Nishimura, Y. Yoshimsa, K. Nakao.: "Increased glucose metabolism and insulin sensitivity in transgenic skinny mice overexpressing leption."Diagbetes. 48:9. 1822-1829 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] M. Shintani, H. Nishimura, T. Akamizu, S. Yonemitsu, H. Masuzaki, Y. Ogawa, K. Hosoda, G, Inoue, Y. Yoshimasa, K. Nakao.: "Thyrotropin decreases leptin production in rat adipocytes."Metabolism. 48:12. 1570-1574 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] K. Nakao, Y. Ogawa, H. Masuzaki, M. Aizawa-Abe, K. Ebihara, N. Matsuoka, N. Satoh, T. Hayashi, K. Hosoda, G. Inoue, Y. Yoshimasa.: "Potential usefulness of leptin for the treatment of diabetes. Common disease : Genetic and pathogenic aspects of multifactorial diseases."Elsevier Science B. V. 21-30 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Y. Yamamoto, Y. Yoshimasa, M. Koh, J. Suga, H. Masuzaki, Y. Ogawa, K. Hosoda, H. Nishimura, Y. Watanabe, G. Inoue, K. Nakao.: "Constitutively active MAP kinase kinase increases GLUT1 expression and recruits both GLUT1 and GLUT4 at the cell surface in 3T3-L1 adipocytes."Diabetes. 49 : 3. 332-339 (2000)
Description
「研究成果報告書概要(欧文)」より
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[Publications] M. Shintani, H. Nishimura, s. Yonemitsu, H. Masuzaki, Y. Oagawa, K. Hosoda, G. Inoue, Y. Yoshimasa, K. Nakao.: "Downregulation of leptin by free fatty acids in rat adipocytes : effects triacsin C, palmitate, and 2-bromopalmitate."Metabolism. 49 : 3. 326-330 (2000)
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「研究成果報告書概要(欧文)」より
