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Oral formulation of angiotensin-(1-7) improves lipid metabolism and prevents high-fat diet-induced hepatic steatosis and inflammation in mice.

Abstract
Angiotensin (Ang)-(1-7) has been described as an important tool on treating and preventing metabolic disorders. In this study, we aimed to evaluate the effect of an oral formulation of Ang-(1-7) included in hydroxypropylβ-cyclodextrin (HPβCD/Ang-[1-7]) on hepatic function, steatosis, and on liver inflammatory markers expression in mice treated with a high-fat diet. Male FVB/N mice were divided into 4 groups and fed for 60 days, with each group receiving 1 of the following diets: standard diet+HPβCD, standard diet+Ang-(1-7)/HPβCD, high-fat diet+HPβCD, or high-fat diet+Ang-[1-7]/HPβCD. Body weight, food intake, and blood parameters, such as total cholesterol, triglyceride, alaninetransaminases, and aspartate transaminases, were evaluated. Immunohistochemical analyses were performed for inflammatory markers tumor necrosis factor-α and interleukin-6. Expression of angiotensin converting enzyme, angiotensin-converting enzyme-2, interleukin-1β, tumor necrosis factor-α, interleukin-6, transforming growth factor-β, acetyl-CoA carboxylase, carbohydrate-responsive element-binding protein, peroxisome proliferator-activated receptor-γ, and sterol regulatory element-binding proteins-1c was evaluated by quantitative real-time polymerase chain reaction. The major findings of our study included reduced liver fat mass and weight, decreased plasma total cholesterol, triglyceride, and alaninetransaminase enzyme levels in the oral Ang-(1-7)-treated groups compared with the control groups. These results were accompanied by a significant reduction in tumor necrosis factor-α and interleukin-6 mRNA expression in the liver. Analyses of liver adipogenesis-related genes by quantitative real-time polymerase chain reaction showed that acetyl-CoA carboxylase, peroxisome proliferator-activated receptor-γ, and sterol regulatory element-binding proteins-1c mRNA expression were significantly suppressed. In conclusion, we observed that treatment with Ang-(1-7) improved metabolism and decreased proinflammatory profile and fat deposition in liver of mice.
AuthorsJohn David Feltenberger, João Marcus Oliveira Andrade, Alanna Paraíso, Lucas Oliveira Barros, Aristides Batista Maia Filho, Ruben D M Sinisterra, Frederico B Sousa, André Luiz Sena Guimarães, Alfredo Mauricio Batista de Paula, Maria José Campagnole-Santos, Mahboob Qureshi, Robson Augusto Souza dos Santos, Sérgio Henrique Sousa Santos
JournalHypertension (Dallas, Tex. : 1979) (Hypertension) Vol. 62 Issue 2 Pg. 324-30 (Aug 2013) ISSN: 1524-4563 [Electronic] United States
PMID23753417 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interleukin-6
  • Peptide Fragments
  • Srebf1 protein, mouse
  • Sterol Regulatory Element Binding Protein 1
  • Tumor Necrosis Factor-alpha
  • Angiotensin I
  • angiotensin I (1-7)
Topics
  • Administration, Oral
  • Angiotensin I (administration & dosage, pharmacology)
  • Animals
  • Chemistry, Pharmaceutical
  • Diet, High-Fat
  • Fatty Liver (prevention & control)
  • Inflammation (prevention & control)
  • Interleukin-6 (physiology)
  • Lipid Metabolism (drug effects)
  • Male
  • Mice
  • Peptide Fragments (administration & dosage, pharmacology)
  • Sterol Regulatory Element Binding Protein 1 (physiology)
  • Tumor Necrosis Factor-alpha (physiology)

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