Efecto del tratamiento con candesartan sobre los mecanismos y factores implicados en el desarrollo de la enfermedad cardiovascular asociada a sobrepeso y exceso de tejido adiposo visceral en la rata

  1. Miana Ortega, María
  2. Heras Jiménez, Natalia de las
  3. Martín Fernández, Beatriz
  4. Ballesteros, Sandra
  5. Valero, María
  6. Martínez, Ernesto
  7. Oubiña, Pilar
  8. Lahera Juliá, Vicente
  9. Cachofeiro Ramos, María Victoria
Journal:
Clínica e investigación en arteriosclerosis

ISSN: 0214-9168 1578-1879

Year of publication: 2011

Volume: 23

Issue: 2

Pages: 55-61

Type: Article

More publications in: Clínica e investigación en arteriosclerosis

Metrics

Cited by

  • Scopus Cited by: 0 (17-02-2024)
  • Web of Science Cited by: 0 (23-10-2023)

SCImago Journal Rank

  • Year 2011
  • SJR Journal Impact: 0.102
  • Best Quartile: Q4
  • Area: Cardiology and Cardiovascular Medicine Quartile: Q4 Rank in area: 312/349
  • Area: Pharmacology (medical) Quartile: Q4 Rank in area: 239/268

Scopus CiteScore

  • Year 2011
  • CiteScore of the Journal : 0.2
  • Area: Pharmacology (medical) Percentile: 14
  • Area: Cardiology and Cardiovascular Medicine Percentile: 13

Abstract

Objective: The renin angiotensin system has been shown to participate in the development of metabolic syndrome. The aim of this study was to determine whether the angiotensin ii type 1 receptor blocker, candesartan, exerts a protective effect against metabolic and vascular abnormalities in rats fed a high fat diet (HFD). Methods: Sprague Dawley rats (n = 30) were divided into three groups: 1) rats fed a standard diet for 7 weeks, used as a control group; 2) rats fed a HFD (33.5% fat) for 7 weeks; and 3) rats fed a HFD (33.5% fat) treated with candesartan (2 mg/kg/day) for 7 weeks. Body weight, white and brown adipose tissue weight, plasma concentrations and protein expression of leptin and adiponectin in white adipose tissue, glucose and lipid metabolism were investigated. Results: HFD rats showed increased body, epididymal and lumbar adipose tissue weights. Candesartan attenuated all of these parameters. The leptin/adiponectin ratio of plasma concentrations and protein expression in lumbar adipose tissue increased in HDF rats, and were normalized by candesartan. Candesartan also improved insulin sensitivity and lipid profile. Conclusion: Correction of the leptin-adiponectin imbalance may be an important mechanism participating in the protective effect of candesartan in HDF rats.