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An Adipocyte-specific Plasma Protein, Adiponectin/GBP28, functions as a mediator of biological defense mechanism.

Research Project

Project/Area Number 16590061
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Biological pharmacy
Research InstitutionTokushima Bunri University (2005)
Showa University (2004)

Principal Investigator

TOMITA Motowo  Tokushima Bunri University, Pharmacy, Professor, 薬学部, 教授 (30102370)

Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
Keywordsadiponectin / gelatin-binding protein / plasma protein / transgenic mice / cold exposure / biological defense / intestinal bleeding / GBP28 / ゼラチン結合蛋白質 / アンチセンストランスジェニックマウス
Research Abstract

Recently, adiponectin/GBP28, a plasma protein which is specifically endocrined with adipose tissue, has been found to have the activities that decreased plasma fatty acids concentration and improve insulin resistance. These activities indicate that adiponectin/GBP28 relates to metabolic syndrome.
In this study, we produced adiponectin/GBP28-transgenic mice (Tg) and anti-transgenic mice (anti-Tg) to investigate whether adiponectin plays a role in regulation of energy homeostasis. While the wild mice expressed adiponectin/GBP28 in adipose tissue only, Tg mice expressed the protein in all tissues. The plasma concentration of adiponectin/GBP28 of Tg mice was higher than that of wild mice during juvenile stage and decreased in the same level as that of wild mice as they grow ; that of anti-Tg mice was always less than that of wild mice. It is notable that mature female mice changed the plasma concentration of adiponectin/GBP28 under the cycle of menstrual period.
Under fasting conditions, anti-Tg mice decreased their body weight faster than wild and Tg mice. Interestingly, the anti-Tg mice tended to die after 48-hr fasting. We also found that the anti-Tg mice significantly reduced locomotion activities and body temperature after 48-hr fasting. Intestinal bleeding which might be caused by bacterial attacking seemed to be the cause of the anti-Tg mice's death. The findings suggested that adiponectin/GBP28 plays a role in biological defense systems as well as regulation of lipid metabolism. Thus, a possibility was considered that the deletion of adiponectin/GBP28 decreased a regulatory response against the changes of environmental conditions.
When anti-Tg mice were exposed under cold circumstance at 5℃, the anti-Tg mice decreased their body temperature faster than wild mice. This results support that the deletion of adiponectin/GBP28 caused the disorder of lipid metabolism to maitain body temperature.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (4 results)

All 2004

All Journal Article (4 results)

  • [Journal Article] タンパク質構造からみたアディポネクチンの生理活性予測2004

    • Author(s)
      富田 基郎
    • Journal Title

      B10 Clinica 19・13

      Pages: 5-5

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Increased serum leptin protects from adiposity despite the increased glucose uptake in white adipose tissue in mice lacking p85alpha phosphoinositide 3-kinase2004

    • Author(s)
      T.Terauchi
    • Journal Title

      Diabetes 53・9

      Pages: 10-10

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Biological functions of adiponectin speculated from protein Structure2004

    • Author(s)
      M.Tomita
    • Journal Title

      BioClinica 19・13

      Pages: 5-5

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] タンパク質構造からみたアディポネクチンの生理活性予測2004

    • Author(s)
      富田基郎
    • Journal Title

      BIO Clinica 19・13

      Pages: 5-5

    • Related Report
      2004 Annual Research Report

URL: 

Published: 2004-04-01   Modified: 2016-04-21  

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