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Study on prevention of fetal abnormalities by maternal diabetes mellitus using transgenic mice overexpressing thioredoxin

Research Project

Project/Area Number 12470214
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionMie University

Principal Investigator

TOYODA Nagayasu  Mie University, Faculty of Medicine, Professor, 医学部, 教授 (40126983)

Co-Investigator(Kenkyū-buntansha) SUGIYAMA Takashi  Mie University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (10263005)
MIYAZAKI Junichi  Osaka University, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (10200156)
Project Period (FY) 2000 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2002: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥9,100,000 (Direct Cost: ¥9,100,000)
Keywordsantioxidant / thioredoxin / gestational diabetes mellitus / congenital abnormality / transgenic mice / diabetes mellitus / 酸化ストレス
Research Abstract

Oxidant stress has been shown to be one of cause for fetal abnormalities in pregnancy complicated by diabetes mellitus. This study was undertaken to assess the mechanism of fetal anmaly in diabetic mother using transgenic mice that ubiquitously overexpress thioredoxin which is one of antioxidant factors.
After mating between transgenic male mice and diabetic female mice, fetuses were examined. Some factors such as body weight, hormonal status and blood glucose levels were compared between transgenic and wild typed fetus.
It took so long time to establish transgenic mice that overexpress thioredoxin. Therefore, we can not get enough results to evaluate analyses so far. We will be able to publish some papers next year.

Report

(4 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • 2000 Annual Research Report
  • Research Products

    (19 results)

All Other

All Publications (19 results)

  • [Publications] Niwa, H., et al.: "Phenotypic complementation establishes requirements for specific POU domain and generic transactivation function of Oct-3/4 in embryonic stem cells"Mol. Cell. Biol.. 22. 1526-1536 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kawaguchi K, et al.: "PPAR-γ, TNF-α Messenger RNA levels and lipase activity in the pregnant and lactating rat"Life Science. 72. 1655-1663 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Iizuka, K., et al.: "Metabolic consequence of long-term exposure of pancreatic β cells to free fatty acid with special reference to glucose insensitivity"Biochem. Biophys. Acta. 1586. 23-31 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hasegawa,S., Sato,T., Akazawa,H., Okada,H., Maeno,A., Ito,M., Sugitani,Y., Shibata,H., Miyazaki,J., Katsuki,M., Yamauchi,Y., Yamamura,K., Katamine,S.& Noda,T.: "Apoptosis in neural crest cells by functional loss of APC tumor suppressor gene"Proc.Natl.Acad.Sci.USA. 99. 297-302 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Iizuka,K., Nakajima,H., Namba,M., Miyagawa,J., Miyazaki,J., Hanafusa,T.& Matsuzawa,Y.: "Metabolic consequence of long-term exposure of pancreatic β cells to free fatty acid with special reference to glucose insensitivity"Biochem.Biophys.Acta. 1586. 23-31 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Niwa,H., Masui,S., Chambers,I., Smith,A.G.& Miyazaki,J.: "Phenotypic complementation establishes requirements for specific POU domain and generic transactivation function of Oct-3/4 in embryonic stem cells"Mol.Cell.Biol.. 22. 1526-1536 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kawaguchi K, Sugiyama T, Hibasami H and Toyoda N.: "PPAR-γ TNF-α Messenger RNA levels and lipase activity in the pregnant and lactating rat"Life Science. 72. 1655-1663 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Sugiyama T, Wang JC, Scott DK, Granner DK: "Transcription activation by the orphan nuclear receptor, chicken ovalbumin upstream promoter-transcription factor I(COUP-TFI), Definition of the domain involved in the glucocorticoid response of the phosphoenolpyruvate carboxykinase gene"Journal of Biological Chemistry. 275(05). 3446-3454 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Ayumi Sugaya, Takashi Sugiyama, Sachiko Yanase, Xiao-Xiong Shen, Hiroyuki Minoura, Nagayasu Toyoda: "Expression of Glucose Transporter 4 mRNA in Adipose Tissue and Skeletal Muscle of Ovariectomized Rats Treated with Sex Steroid Hormones"Life Sciences. 66(7). 641-648 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Niwa, H., et al.: "Phenotypic complementation establishes requirements for specific POU domain and generic transactivation function of Oct-3/4 in embryonic stem cells"Mol. Cell. Biol.. 22. 1526-1536 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Kawaguchi k, et al.: "PPAR-γ, TNF-α Messenger RNA levels and lipase activity in the pregnant and lactating rat"Life Science. 72. 1655-1663 (2003)

    • Related Report
      2002 Annual Research Report
  • [Publications] Iizuka, K., et al.: "Metabolic consequence of long-term exposure of pancreatic β cells to free fatty acid with special reference to glucose insensitivity"Biochem. Biophys. Acta. 1586. 23-31 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Iizuka K: "Metabolic consequence of long-term exposure of pacreatic β cells to free fatty acid with special reference to glucose insensitivity"Biochem.Biophys.Acta. 1586. 23-31 (2002)

    • Related Report
      2001 Annual Research Report
  • [Publications] Nitta Y: "IL-12 plays a pathologic role in the development of diabetes in NOD mice"J.Autoimmun.. 16. 97-104 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Iizuka K., et al.: "Stable overexpression of the glucose-6-phosphatase catalytic subunit attenuates glucose sensitivity of insulin secretion from a mouse pancreatic beta-cell line."J.Endocrinol.. 164. 307-314 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Hotta M., et al.: "Oxidative stess and pancreatic b-cell destruction in insulin-dependent diabetes mellitus."In Antioxidants in Diabetes Management. 265-274 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Nitta Y., et al.: "IL-12 plays a pathologic role in the development of diabetes in NOD mice."J.Autoimmunity. (in press).

    • Related Report
      2000 Annual Research Report
  • [Publications] Sugaya A., et al.: "Expression of Glucose Transporter 4 mRNA in Adipose Tissue and Skeletal Muscle of Ovariectomized Rats Treated with Sex Steroid Hormones."Life Sciences. 66. 641-648 (2000)

    • Related Report
      2000 Annual Research Report
  • [Publications] Sugaya A., et al.: "Comparison of the validity of the criteria for gestational diabetes mellitus by WHO and by the Japan Society of Obstetrics and Gynecology by the outcomes of pregnancy."Diabetes Research and Clinical Practice. 50. 57-63 (2000)

    • Related Report
      2000 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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