Aminoguanidine Prevents Diabetes-Induced Arterial Wall Protein Cross-Linking

  • M. Brownlee
    Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
  • H. Vlassara
    Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
  • A. Kooney
    Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
  • P. Ulrich
    Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
  • A. Cerami
    Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.

抄録

<jats:p>Age-associated increases in collagen cross-linking and accumulation of advanced glycosylation products are both accelerated by diabetes, suggesting that glucose-derived cross-link formation may contribute to the development of chronic diabetic complications as well as certain physical changes of aging. Aminoguanidine, a nucleophilic hydrazine compound, prevented both the formation of fluorescent advanced nonenzymatic glycosylation products and the formation of glucose-derived collagen cross-links in vitro. Aminoguanidine administration to rats was equally effective in preventing diabetes-induced formation of fluorescent advanced nonenzymatic glycosylation products and cross-linking of arterial wall connective tissue protein in vivo. The identification of aminoguanidine as an inhibitor of advanced nonenzymatic glycosylation product formation now makes possible precise experimental definition of the pathogenetic significance of this process and suggests a potential clinical role for aminoguanidine in the future treatment of chronic diabetic complications.</jats:p>

収録刊行物

  • Science

    Science 232 (4758), 1629-1632, 1986-06-27

    American Association for the Advancement of Science (AAAS)

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