title: Improved lipid and glucose metabolism in transgenic rats with increased circulating angiotensin-(1-7).
abstract: OBJECTIVE
  Obesity and diabetes remain among the world's most pervasive health problems. Although the importance of angiotensin II for metabolic regulation is well documented, the role of the angiotensin-(1-7)/Mas axis in this process is poorly understood. The aim of this study was to evaluate the effect of increased angiotensin-(1-7) plasma levels in lipid and glucose metabolism using transgenic rats that express an angiotensin-(1-7)-releasing fusion protein, TGR(A1-7)3292 (TGR).
  
  
  RESULTS
  The increased angiotensin-(1-7) levels in TGR induced enhanced glucose tolerance, insulin sensitivity, and insulin-stimulated glucose uptake. In addition, TGR presented decreased triglycerides and cholesterol levels, as well as a significant decrease in abdominal fat mass, despite normal food intake. These alterations were accompanied by a marked decrease of angiotensinogen expression and increased Akt in adipose tissue. Furthermore, augmented plasma levels and expression in adipose tissue was observed for adiponectin. Accordingly, angiotensin-(1-7) stimulation increased adiponectin production by primary adipocyte culture, which was blocked by the Mas antagonist A779. Circulating insulin and muscle glycogen content were not altered in TGR.
  
  
  CONCLUSIONS
  These results show that increased circulating angiotensin-(1-7) levels lead to prominent changes in glucose and lipid metabolism.
authors.affiliation: Laboratory of Hypertension, INCT-NanoBiofar, Minas Gerais, Brazil.
authors.forename: Sérgio Henrique S
authors.initials: SH
authors.lastname: Santos
authors.forename: Janaina Felix
authors.initials: JF
authors.lastname: Braga
authors.forename: Erica Guilhen
authors.initials: EG
authors.lastname: Mario
authors.forename: Laura Cristina J
authors.initials: LC
authors.lastname: Pôrto
authors.forename: Maria da Glória
authors.initials: Mda G
authors.lastname: Rodrigues-Machado
authors.forename: Antonela
authors.initials: A
authors.lastname: Murari
authors.forename: Leida Maria
authors.initials: LM
authors.lastname: Botion
authors.forename: Natalia
authors.initials: N
authors.lastname: Alenina
authors.forename: Michael
authors.initials: M
authors.lastname: Bader
authors.forename: Robson Augusto S
authors.initials: RA
authors.lastname: Santos
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D050154:Adiposity; D000803:Angiotensin I; D000804:Angiotensin II / Q000031:analogs & derivatives / Q000097:blood* / Q000235:genetics / Q000494:pharmacology; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001835:Body Weight; D002478:Cells, Cultured; D002784:Cholesterol / Q000097:blood; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics; D008297:Male; D010446:Peptide Fragments / Q000097:blood* / Q000235:genetics / Q000494:pharmacology; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D055647:Rats, Transgenic; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000378:metabolism; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D015854:Up-Regulation
chemical_list: C092006:7-Ala-angiotensin (1-7); D052242:Adiponectin; C499920:Adipoq protein, rat; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D014280:Triglycerides; D000804:Angiotensin II; D000803:Angiotensin I; D002784:Cholesterol; D051057:Proto-Oncogene Proteins c-akt; C118790:angiotensin I (1-7)