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Role of advanced glycation end-product in the development and progression of diabetic nephropathy.

Research Project

Project/Area Number 07671252
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionOkayama University

Principal Investigator

MAKINO Hirofumi  Okayama University Medical School, assistant, 医学部, 教授 (50165685)

Co-Investigator(Kenkyū-buntansha) YAMAJI Hiroaki  Okayama University Hospital, 医学部・附属病院, 医員
HORIUCHI Masakimi  Kumamoto University Medical School, professor, 医学部, 教授 (10117377)
SHIKATA Kenichi  Okayama University Medical School, assistant, 医学部, 助手 (00243452)
Project Period (FY) 1995 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
Keywordsdiabetes mellitus / kidney / AGE / Maillard reaction / extracellular matrix / 糖化反応最終産物 / 糖尿病性腎症 / 糖化反応 / メサンギウム細胞 / 糸球体 / 血管合併症
Research Abstract

In diabetic state, glycation reaction of the proteins (Maillard reaction) undergoes and advanced glycation endproduct (AGE) accumulates in varous tissues. AGEs bind to the their receptors on the macrophages, and are known to induce the production of cytokines and nitric oxide (NO). Extracellular matrix with AGE modification is resistant to the proteolytic degradation. To explore the role of AGEs in the progression of the diabetic nephropathy, immunohistochemical studies of AGE and extracellular matrix components were performed in the kidney biopsy specimens of diabetic nephropathy patients, streptozotocin-induced diabetic rat kidney, and OLETF rat. In the mesangial area and tubules, AGEs were accumulated in the diabetic kidney. Especially in the nodular lesions of the diabetic kidneys, AGE were noted. By ultra-high resolution scanning electron microscopy showed enlarged meshwork of mesangial matrix of nodular lesions. These results indicated that AGEs accumulated with the progression of the diabetic nephropathy. AGEs may bind to the receptor on the mesangial cells and thus stimulate the production and inhibit the proteolytic degradations. AGEs may play a pivotal role in the alterations of the structual architecture of the extracellular matrix and glomerulosclerosis of the diabetic nephropathy.

Report

(3 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • Research Products

    (25 results)

All Other

All Publications (25 results)

  • [Publications] Makino H et al: "Ultrastructure of nononzymatically glycated mesangial matrix in diabetic nephropathy" Kidney International. 48. 517-526 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Shikata K. et al: "Locarization of advanced glycation endproduct in the kidney of experimental diabeticrats" J.Diaberi Compli. 9. 269-271 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Sugimoto H. et al: "Increased gene expression of insulin like growth factor-1 receptor in experimental diabetic rat glomeruli" Nephron. 72. 648-653 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H. et al: "Phenotypic modulation of the mesangium reflected by contractile proteins in dinbetes" Diabetes.45. 488-495 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.: "Abnormalities of extracellutar matrix and their mechanism in diabetic nephropathy." Therapewri Research. 16. 2627-2631 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al: "AGE and tubular injuries in dinbetic nephropathy." Endocrinology and Diabetology. 3. 512-578 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.: "Mechanism of development and progression of diabetic nephropathy" Diabetes Journal. 25. 1-7 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.: "Etiology of diabetic nephropathy" Clinical Nutrition. 90. 546-553 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy" Kidney International. 48. 517-526 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Shikata K.et al.: "Locarization of advanced glycation endproduct in the kidney of experimental diabetic rats." J Diabetes Compl. 9. 269-271 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Sugimoto H et al.: "Increased gene expression of insulin like growth factor-1 receptor in experimental diabetic rat glomeruli" Nephron. 72. 648-653 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "Phenotypic modulation of the mesangium reflected by contractile proteins in diabetes." Diabetes. 45. 488-495 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.: "Abnormalities of extracellular matrix and their mechanism in diabetic nephropathy" Therapeutic Research. 16. 2627-2631 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "AGE and tubular injuries in diabetic nephropathy" Endocrinology and Diabetology. 3. 512-518 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "Mechanism of development and progression of diabetic nephropathy" Diabetes Journal. 25. 1-7 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "Etiology of diabetic nephropathy" Clinical Nutrition Research. 90. 546-553 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Makino H.et al.: "Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy." Kidney International. 48. 517-526 (1995)

    • Related Report
      1996 Annual Research Report
  • [Publications] Shikata K.at al.: "Localization of advanced glycation endproducts in the kidney of experimental diabetic rats." J.Diabetes and Its Complications. 9. 632-638 (1995)

    • Related Report
      1996 Annual Research Report
  • [Publications] 槙野博史他: "糖尿病性腎症概論 病理と形態" 糖尿病と透析療法. 53-63 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] 弘中一江他: "糖尿病性腎症の糸球体病変-免疫組織化学および電顕的検討-" Diabetes Frontier. 7. 521-526 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] 槙野博史他: "糖尿病性腎症における尿細管異常とAGE" 内分泌・糖尿病科. 3. 512-518 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] 槙野博史他: "腎傷害を伴う糖尿病の治療" Medical Practice. 13. 923-927 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] Makino H et al: "Ultrastructure of nonenzymatically glycated mesangial matrix in diabetic nephropathy." Kidney Int.48. 517-526 (1995)

    • Related Report
      1995 Annual Research Report
  • [Publications] Shikata K et al: "Localization of advanced glycation end products in the kidney of experimental diabetic rats." J.Diabetes Compli.9. 269-271 (1995)

    • Related Report
      1995 Annual Research Report
  • [Publications] 植野博史: "糖尿病性腎症における細胞外基質異常とそのメカニズム," Therapeutic research,. 16. 2627-2631 (1995)

    • Related Report
      1995 Annual Research Report

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Published: 1995-04-01   Modified: 2016-04-21  

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