| Expression pattern of thermogenesis-related factors in interscapular brown adipose tissue of alloxan-treated rats: beneficial effect of L-arginine. | |
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MedLine Citation:
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PMID: 20403454 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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A Vasilijević; Lj Vojcić; I Dinulović; B Buzadzić; A Korać; V Petrović; A Janković; B Korać |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-18 |
Journal Detail:
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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:
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Created Date: 2010-05-20 Completed Date: 2010-09-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9709307 Medline TA: Nitric Oxide Country: United States |
Other Details:
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Languages: eng Pagination: 42-50 Citation Subset: IM |
Copyright Information:
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Copyright (c) 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Physiology, Institute for Biological Research, Sinisa Stanković, University of Belgrade, Bulevar Despota Stefana 142, 11060 Belgrade, Serbia. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue, Brown
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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:
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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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