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Abstract Title:

Beneficial effects of L-arginine nitric oxide-producing pathway in rats treated with alloxan.

Abstract Source:

J Physiol. 2007 Nov 1;584(Pt 3):921-33. Epub 2007 Aug 23. PMID: 17717015

Abstract Author(s):

Ana Vasilijevic, Biljana Buzadzic, Aleksandra Korac, Vesna Petrovic, Aleksandra Jankovic, Bato Korac

Article Affiliation:

Department of Physiology, Institute for Biological Research, Sinia Stankovi, University of Belgrade, Bulevar Despota Stefana 142, 11060, Belgrade, Serbia.

Abstract:

In an attempt to elucidate molecular mechanisms and factors involved in beta cell regeneration, we evaluated a possible role of the L-arginine-nitric oxide (NO)-producing pathway in alloxan-induced diabetes mellitus. Diabetes was induced in male Mill Hill rats with a single alloxan dose (120 mg kg(-1)). Both non-diabetic and diabetic groups were additionally separated into three subgroups: (i) receiving L-arginine . HCl (2.25%), (ii) receiving L-NAME . HCl (0.01%) for 12 days as drinking liquids, and (iii) control. Treatment of diabetic animals started after diabetes induction (glucose level>or = 12 mmol l(-1)). We found that disturbed glucose homeostasis, i.e. blood insulin and glucose levels in diabetic rats was restored after L-arginine treatment. Immunohistochemical findings revealed that L-arginine had a favourable effect on beta cell neogenesis, i.e. it increased the area of insulin-immunopositive cells. Moreover, confocal microscopy showed colocalization of insulin and pancreas duodenum homeobox-1 (PDX-1) in both endocrine and exocrine pancreas. This increase in insulin-expressing cells was accompanied by increased cell proliferation (observed by proliferating cell nuclear antigen-PCNA immunopositivity) which occurred in a regulated manner since it was associated with increased apoptosis (detected by the TUNEL method). Furthermore, L-arginine enhanced both nuclear factor-kB (NF-kB) and neuronal nitric oxide synthase (nNOS) immunopositivities. The effect of L-arginine on antioxidative defence was observed especially in restoring to control level the diabetes-induced increase in glutathione peroxidase activity. In contrast to L-arginine, diabetic pancreas was not affected by L-NAME supplementation. In conclusion, the results suggest beneficial L-arginine effects on alloxan-induced diabetes resulting from the stimulation of beta cell neogenesis, including complex mechanisms of transcriptional and redox regulation.

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Sayer Ji
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