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

Matthew B. West, Kota V. Ramana, Karin Kaiserova, Satish K. Srivastava, Aruni Bhatnagar

Research output: Contribution to journalArticle

20 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)2609-2614
Number of pages6
JournalFEBS Letters
Volume582
Issue number17
DOIs
StatePublished - Jul 23 2008

Keywords

  • Cell adhesion molecule
  • Diabetes mellitus
  • Inflammation
  • Nitric oxide
  • Signal transduction

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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  • Cite this

    West, M. B., Ramana, K. V., Kaiserova, K., Srivastava, S. K., & Bhatnagar, A. (2008). l-Arginine prevents metabolic effects of high glucose in diabetic mice. FEBS Letters, 582(17), 2609-2614. https://doi.org/10.1016/j.febslet.2008.06.039