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High-Fat Diet-Induced Obesity Model Does Not Promote Endothelial Dysfunction via Increasing Leptin/Akt/eNOS Signaling.
Rocha, Vanessa da Silva; Claudio, Erick Roberto Gonçalves; da Silva, Vitor Loureiro; Cordeiro, Jóctan Pimentel; Domingos, Lucas Furtado; da Cunha, Márcia Regina Holanda; Mauad, Helder; do Nascimento, Thiago Bruder; Lima-Leopoldo, Ana Paula; Leopoldo, André Soares.
Afiliação
  • Rocha VDS; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • Claudio ERG; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Brazil.
  • da Silva VL; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • Cordeiro JP; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • Domingos LF; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • da Cunha MRH; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • Mauad H; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Brazil.
  • do Nascimento TB; Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA, United States.
  • Lima-Leopoldo AP; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
  • Leopoldo AS; Physiology and Biochemistry Laboratory, Department of Sports, Center of Physical Education and Sports, Federal University of Espírito Santo, Vitória, Brazil.
Front Physiol ; 10: 268, 2019.
Article em En | MEDLINE | ID: mdl-30949067
Experimental studies show that the unsaturated high-fat diet-induced obesity promotes vascular alterations characterized by improving the endothelial L-arginine/Nitric Oxide (NO) pathway. Leptin seems to be involved in this process, promoting vasodilation via increasing NO bioavailability. The aim of this study was to test the hypothesis that unsaturated high-fat diet-induced obesity does not generate endothelial dysfunction via increasing the vascular leptin/Akt/eNOS signaling. Thirty-day-old male Wistar rats were randomized into two groups: control (C) and obese (Ob). Group C was fed a standard diet, while group Ob was fed an unsaturated high-fat diet for 27 weeks. Adiposity, hormonal and biochemical parameters, and systolic blood pressure were observed. Concentration response curves were performed for leptin or acetylcholine in the presence or absence of Akt and NOS inhibitor. Our results showed that an unsaturated high-fat diet promoted a greater feed efficiency (FE), elevation of body weight and body fat (BF), and an adiposity index, characterizing a model of obesity. However, comorbidities frequently associated with experimental obesity were not visualized, such as glucose intolerance, dyslipidemia and hypertension. The evaluation of the endothelium-dependent relaxation with acetylcholine showed no differences between the C and Ob rats. After NOS inhibition, the response was completely abolished in the Ob group, but not in the C group. Furthermore, Akt inhibition completely blunted vascular relaxation in the C group, but not in the Ob group, which was more sensitive to leptin-induced vascular relaxation. L-NAME incubation abolished the relaxation in both groups at the same level. Although Akt inhibitor pre-incubation reduced the leptin response, group C was more sensitive to its effect. In conclusion, the high-unsaturated fat diet-induced obesity improved the vascular reactivity to leptin and does not generate endothelial dysfunction, possibly by the increase in the vascular sensitivity to leptin and increasing NO bioavailability. Moreover, our results suggest that the increase in NO production occurs through the increase in NOS activation by leptin and is partially mediated by the Akt pathway.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Clinical_trials Idioma: En Revista: Front Physiol Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Brasil País de publicação: Suíça

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Clinical_trials Idioma: En Revista: Front Physiol Ano de publicação: 2019 Tipo de documento: Article País de afiliação: Brasil País de publicação: Suíça