FEBS Letters
Volume 582, Issue 17 , Pages 2609-2614, 23 July 2008

l-Arginine prevents metabolic effects of high glucose in diabetic mice

Edited by Judit Ovádi

  • Matthew B. West

      Affiliations

    • Institute of Molecular Cardiology and Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY 40202, United States
    • ,
  • Kota V. Ramana

      Affiliations

    • Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, United States
    • ,
  • Karin Kaiserova

      Affiliations

    • Institute of Molecular Cardiology and Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY 40202, United States
    • ,
  • Satish K. Srivastava

      Affiliations

    • Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, United States
    • ,
  • Aruni Bhatnagar

      Affiliations

    • Institute of Molecular Cardiology and Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY 40202, United States
    • Corresponding Author InformationCorresponding author. Address: University of Louisville, Division of Cardiology, Department of Medicine, Delia Baxter Building, 580 South Preston Street, Room 421F, Louisville, KY 40202, United States. Fax: +1 502 852 3663.

Received 7 May 2008; received in revised form 10 June 2008; accepted 19 June 2008. published online 27 June 2008.

Abstract 

We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-βII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.

Keywords: Nitric oxide, Diabetes mellitus, Cell adhesion molecule, Signal transduction, Inflammation

 

PII: S0014-5793(08)00552-8

doi:10.1016/j.febslet.2008.06.039

FEBS Letters
Volume 582, Issue 17 , Pages 2609-2614, 23 July 2008

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