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Regul Pept ; 178(1-3): 64-70, 2012 Oct 10.
Article in English | MEDLINE | ID: mdl-22749992

ABSTRACT

INTRODUCTION: The aim of the present study was to evaluate the effect of a transgenic-induced chronic increase of Ang-(1-7) on the expression of inflammatory markers in adipose tissue and the metabolic profile in rats treated with high-fat diet. RESEARCH DESIGN AND METHODS: Transgenic rats expressing an Ang-(1-7)-producing fusion protein (TGR L-3292) and Sprague Dawley (SD) control rats 4 weeks old were treated for 8 weeks with a high-fat diet. Food intake and body weight were measured once a week. Glucose-tolerance and insulin sensitivity tests were performed one week before the sacrifice. At the end of the experiment plasma lipid concentrations were measured in TGR and SD rats. Adipose tissue were weighted and corrected by the body weight. Proinflammatory markers in adipose tissue were analyzed using Western-blotting, real time-PCR and immunohistochemistry. RESULTS: High-fat diet TGR rats presented increased HDL cholesterol levels and decreased abdominal fat mass, without changes in food intake. In addition, rats with increased Ang-(1-7) levels had lower body weight. Molecular analysis revealed decreased IL-1ß and COX-2 in adipose tissue. CONCLUSIONS: Taken together, these results show that chronic high circulating angiotensin-(1-7) levels protect against metabolic stress induced by a high-fat diet decreasing the proinflammatory profile of adipose tissue.


Subject(s)
Angiotensin I/blood , Diet, High-Fat/adverse effects , Inflammation Mediators/metabolism , Intra-Abdominal Fat/pathology , Peptide Fragments/blood , Adipokines/blood , Adiposity , Animals , Blood Glucose , Cholesterol, HDL/blood , Epididymis/metabolism , Epididymis/pathology , Inflammation , Interleukin-1beta/genetics , Interleukin-1beta/metabolism , Intra-Abdominal Fat/metabolism , Male , Obesity/blood , Obesity/etiology , Obesity/pathology , Oxidative Stress , Rats , Rats, Sprague-Dawley , Rats, Transgenic , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism
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