title: Increased circulating angiotensin-(1-7) protects white adipose tissue against development of a proinflammatory state stimulated by a high-fat diet.
abstract: BACKGROUND
  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.
  
  
  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-1β 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.
authors: National Institute of Science and Technology (INCT-NanoBiofar), Physiology Department, Biological Sciences Institute (ICB), Federal University of Minas Gerais (UFMG), Belo Horizonte, MG, Brazil. sergiosousas@hotmail.com
authors: Sérgio Henrique S
authors: SH
authors: Santos
authors: Luciana Rodrigues
authors: LR
authors: Fernandes
authors: Camila Santos
authors: CS
authors: Pereira
authors: André L Senna
authors: AL
authors: Guimarães
authors: Alfredo M B
authors: AM
authors: de Paula
authors: Maria José
authors: MJ
authors: Campagnole-Santos
authors: Jacqueline Isaura
authors: JI
authors: Alvarez-Leite
authors: Michael
authors: M
authors: Bader
authors: Robson Augusto S
authors: RA
authors: Santos
mesh_terms: D054392:Adipokines / Q000097:blood; D050154:Adiposity; D000803:Angiotensin I / Q000097:blood*; D000818:Animals; D001786:Blood Glucose; D008076:Cholesterol, HDL / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects*; D004822:Epididymis / Q000378:metabolism / Q000473:pathology; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009765:Obesity / Q000097:blood / Q000209:etiology / Q000473:pathology; D018384:Oxidative Stress; D010446:Peptide Fragments / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley; D055647:Rats, Transgenic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D054392:Adipokines; D001786:Blood Glucose; D008076:Cholesterol, HDL; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D010446:Peptide Fragments; D014409:Tumor Necrosis Factor-alpha; D000803:Angiotensin I; C118790:angiotensin I (1-7)