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Study on the associated regulation of energy and metabolism of glucose and lipids

Research Project

Project/Area Number 10470235
Research Category

Grant-in-Aid for Scientific Research (B).

Allocation TypeSingle-year Grants
Section一般
Research Field Metabolomics
Research InstitutionResearch Institute for Production Development

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)

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)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 1999: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥10,000,000 (Direct Cost: ¥10,000,000)
Keywordsenergy metabolism / leptin / insulin / transgenic mouse / UCP3 / insulin sensitivity / エネルギー代謝 / 糖脂質代謝 / インスリン作用 / 肥満 / 糖尿病
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.

Report

(3 results)
  • 2001 Final Research Report Summary
  • 1999 Annual Research Report
  • 1998 Annual Research Report
  • Research Products

    (35 results)

All Other

All Publications (35 results)

  • [Publications] Tanaka T, et al.: "Down regulation of peroxisome proliferator-activatec gamma expression by inflammatory cytokines and its reversal by thiazolidinediones"Diabetologia. 42(6). 702-710 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Masuzaki H, et al.: "Glucose metabolism and insulin sensitivity in transgenic mice overexpressing leptin with lethal yellow agouti mutation : usefulness of leptin for the treatment of obesity-associated diabetes"Diabetes. 48(8). 1615-1622 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Ogawa Y, et al.: "Increased glucose metabolism and insulin sensitivity in transgenic skinny mice overexpressing leptin"Diabetes. 48(9). 1822-1829 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Shintani M, et al.: "Thyrotropin decreases leptin production in rat adipocytes"Metabolism. 48(12). 1570-1574 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Inoue G, et al.: "Development of an in vitro reconstitution assay for glucose transporter 4 translocation"Proc.Natl.Acad.Sci.U.S.A.. 96(26). 14919-14924 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Yamamoto Y, et al.: "Constitutively active MAP kinase kinase increases GLUT1 expression and recruits both GLUTi 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(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Shintani M, et al.: "Downregulation of leptin by free fatty acids in rat adipocytes : effects of triacsin C, palmitate, and 2-bromopalmitate"Metabolism. 49(3). 326-330 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Nakao K, et al.: "Common disease : Genetic and pathogenic aspects of multifactorial diseases Potential usefulness of leptin for the treatment of diabetes"Elsevier Science B.V.. 21-30 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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
    • Related Report
      2001 Final Research Report Summary
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] G. Inoue, B. Cheatham, C. R. Kahn.: "Development of an in vitro reconstitution assay for glucose transpoter 4 translocation."Proc. Natl. Acad. Sci. USA. 96 : 26. 14919-14924 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [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
    • Related Report
      2001 Final Research Report Summary
  • [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)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] T.Tanaka: "Down regulation of peroxisome proliferator-activated receptorgamma expression by inflammatory cytokines and its reversal by thiazolidinediones"Diabetologia. 42:6. 702-710 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] H.Matsuzaki: "Glucose metabolism and insulin sensitivity in transgenic mice overexpressing leptin with lethal yellow agouti mutation"Diabetes. 48:8. 1615-1622 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] H.Matsuzaki: "Increased glucose metabolism and insulin sensitivity in transgenic skinny mice overexpressing leptin"Diabetes. 48:9. 1822-1829 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] M.Shintani: "Thyrotropin decreases leptin production in rat adipocytes"Metabolism. 48:12. 1570-1574 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] G.Inoue: "Development of an in vitro reconstitution assay for glucose transporter 4 translocation"Proc.Natl.Acad.Sci.U.S.A.. 96:26. 14919-14924 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] Y.Yamamoto: "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)

    • Related Report
      1999 Annual Research Report
  • [Publications] K.Nakao: "Common disease : Genetic and pathogenic aspects of multifactorial diseases"Elsevier Science B.V.. 21-30 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] Gen Inoue: "Dynamics of Insulin Signaling in 3T3-L1 Adipocytes:Differential Compartmentalization and Trafficking of IRS-1 and IRS-2." J.Biol.Chem.273. 11548-11555 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Junichi Matsuda: "Increased adipose expression of the uncoupling protein-3 gene by thiazolidinediones in Wistar fatty rats and in cultured adipocytes." Diabetes. 47. 1809-1814 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Tokuji Tnaka: "Down-regulation of peroxisome proliferator-activated receptor γ expression by inflammatory cytokines and its reversal by thiazolidinediones." Diabetologia. in press. (1999)

    • Related Report
      1998 Annual Research Report
  • [Publications] 井上 元: "インスリンによる糖輸送促進機構" 専門医のための糖尿病レビュー'98-最新主要文献と解説-. 49-56 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 井上 元: "エネルギー代謝調節機構" 最新医学 10月増刊号 臨床遺伝学'98. 第53巻. 203-212 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 益崎裕章: "レプチン過剰発現トランスジェニックマウスの作製と糖代謝調節におけるレプチンの意義" 日本肥満学会誌 肥満研究. 第4巻第4号. 15-20 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 益崎裕章: "成人病を解く遺伝子-肥満(レプチンを中心に)-" 診断と治療. 86. 2023-2030 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 益崎裕章: "肥満の分子病態-エネルギー代謝調節の新しい分子医学-" Cardiac Practice. 9(4). 29-35 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 益崎裕章: "レプチン過剰発現モデルとその病態" バイオクリニカ. 13(12). 24-28 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 松田淳一: "骨格筋と褐色脂肪組織に高発現するラット脱共役蛋白質cDNAのクローニングと遺伝子発現の検討" 日本肥満学会誌 肥満研究. 4(3). 31-35 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 小川佳宏: "レプチンの糖代謝調節作用 レプチン過剰発現トランスジェニックマウスより得られた知見" Diabetes Frontier. 9(6). 748-751 (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] 細田公則: "脱共役タンパク質ファミリーの分子機構とエネルギー代謝における臨床的意義" 最新医学. 54. 67-74 (1999)

    • Related Report
      1998 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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