Document Detail


Expression pattern of thermogenesis-related factors in interscapular brown adipose tissue of alloxan-treated rats: beneficial effect of L-arginine.
MedLine Citation:
PMID:  20403454     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Metabolic abnormalities underlying diabetes can be abrogated by L-arginine. Here we examined the molecular basis of disturbed interscapular brown adipose tissue (IBAT) thermogenesis and the possible role of nitric oxide (NO) in the IBAT of diabetic rats. To induce diabetes, adult Mill Hill hybrid hooded male rats were given a single alloxan dose (120 mg/kg). Both non-diabetic and diabetic groups were further divided into three subgroups receiving: (i) L-arginine.HCl (2.25%) or (ii) N(omega)-nitro-L-arginine methyl ester (L-NAME.HCl, 0.01%) for 12 days in drinking water and (iii) untreated controls. Treatment of the diabetic animals started after diabetes induction (glucose level 12 mmol/L). Diabetes led to a decrease in the mRNA levels of uncoupling protein 1 (UCP1), peroxisomal proliferator activator receptor gamma (PPARgamma) and endothelial NO synthase (eNOS) as revealed by RT-PCR. The diabetic rats had reduced eNOS and inducible NOS (iNOS) protein contents accompanied by low tissue vascularization, a parameter directly related to tissue thermogenic state. Downregulation of glutathione peroxidase (GSH-Px) and catalase (CAT) transcripts were also observed in diabetes. In contrast, the expression level of PPARgamma coactivator-1alpha (PGC-1alpha) mRNA was elevated. Supplementation with L-arginine not only restored diabetes-induced changes in the expressions of these molecules important for IBAT regulation, but also increased the vascularity. Interestingly, L-NAME induced similar patterns of changes in vascularity and PGC-1alpha mRNA level as did l-arginine. In summary, our results provide insight into the molecular basis underlying diabetes-induced metabolic and functional disturbances in the IBAT and suggest a beneficial role for the L-arginine-NO production pathway.
Authors:
A Vasilijević; Lj Vojcić; I Dinulović; B Buzadzić; A Korać; V Petrović; A Janković; B Korać
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-18
Journal Detail:
Title:  Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society     Volume:  23     ISSN:  1089-8611     ISO Abbreviation:  Nitric Oxide     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-09-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9709307     Medline TA:  Nitric Oxide     Country:  United States    
Other Details:
Languages:  eng     Pagination:  42-50     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2010 Elsevier Inc. All rights reserved.
Affiliation:
Department of Physiology, Institute for Biological Research, Sinisa Stanković, University of Belgrade, Bulevar Despota Stefana 142, 11060 Belgrade, Serbia.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue, Brown / drug effects*,  metabolism*
Alloxan
Analysis of Variance
Animals
Antioxidants / metabolism
Arginine / pharmacology*
Back
Body Weight / drug effects
Catalase / genetics,  metabolism
Diabetes Mellitus, Experimental / metabolism*
Glutathione Peroxidase / genetics,  metabolism
Ion Channels / genetics,  metabolism
Male
Mitochondrial Proteins / genetics,  metabolism
Nitric Oxide Synthase Type II / metabolism
Nitric Oxide Synthase Type III / metabolism
PPAR gamma / genetics,  metabolism
RNA-Binding Proteins / genetics,  metabolism
Rats
Regional Blood Flow
Thermogenesis / drug effects*
Transcription Factors / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Ion Channels; 0/Mitochondrial Proteins; 0/PPAR gamma; 0/Ppargc1a protein, rat; 0/RNA-Binding Proteins; 0/Transcription Factors; 0/mitochondrial uncoupling protein; 50-71-5/Alloxan; 74-79-3/Arginine; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos2 protein, rat; EC 1.14.13.39/Nos3 protein, rat

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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