High-fat and combined high-fat and sucrose diets promote cardiac oxidative stress independent of Nox2 redox regulation and obesity in rats

Nenhuma Miniatura disponível

Data

2021-01-01

Autores

Gasparini, Patrícia Vasconcelos Fontana
Matias, Amanda Martins
Torezani-Sales, Suellem
Kobi, Jéssika Butcovsky Botto Sarter
Siqueira, Juliana Silva [UNESP]
Corrêa, Camila Renata [UNESP]
Leopoldo, Ana Paula Lima
Leopoldo, André Soares

Título da Revista

ISSN da Revista

Título de Volume

Editor

Resumo

Background/Aims: Oxidative stress is associated with cardiometabolic alterations, and the involvement of excess glucose and fatty acids has been demonstrated in this process. Thus, the aim of this study was to investigate the effects of different hypercaloric diets on cardiac oxidative stress. Methods: Wistar rats were randomized into four groups: control (C), high-sucrose (HS), high-fat (HF), and high-fat with sucrose (HFS). Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Cardiac oxidative stress was analyzed by malondialdehyde (MDA) and carbonylated proteins, and the cardiac protein expression levels of type 1 angiotensin receptor (AT-1), nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2), superoxide dismutase (SOD 1 e 2), glutathione peroxidase (GPX), and catalase (CAT) were determined by western blot. Results: The HF group showed an increase in adiposity; however, it did not present adipocyte hypertrophy and comorbidities. Cardiac MDA and carbonylated protein levels were higher in the HF and HFS compared with the C group. The levels of oxidant and antioxidant proteins showed no difference between the groups. Conclusion: HF and HFS dietary interventions promoted cardiac oxidative stress, in the presence and absence of obesity, respectively. However, this process was neither mediated by the pro-oxidants AT1 and Nox2, nor by the quantitative reduction of antioxidant enzymes.

Descrição

Palavras-chave

1 angiotensin receptor, Cardiac, Hypercaloric diets, Nox2, Oxidative stress

Como citar

Cellular Physiology and Biochemistry, v. 55, n. 5, p. 618-634, 2021.

Coleções