Postgraduate Program in Nutrition and Health, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
São Paulo State University (UNESP), Medical School, Botucatu, São Paulo, Brazil.
Cell Physiol Biochem. 2021 Oct 27;55(5):618-634. doi: 10.33594/000000441.
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.
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.
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.
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.
背景/目的：氧化应激与心脏代谢改变有关，过量的葡萄糖和脂肪酸在此过程中起作用。因此，本研究旨在探讨不同高卡路里饮食对心脏氧化应激的影响。
Wistar 大鼠随机分为 4 组：对照组（C）、高蔗糖（HS）、高脂肪（HF）和高糖高脂肪（HFS）。进行营养评估、食物分析、组织学分析、合并症和心血管特征分析。通过丙二醛（MDA）和羰基化蛋白分析心脏氧化应激，通过 Western blot 测定心脏 1 型血管紧张素受体（AT-1）、烟酰胺腺嘌呤二核苷酸磷酸氧化酶 2（Nox2）、超氧化物歧化酶（SOD1 和 SOD2）、谷胱甘肽过氧化物酶（GPX）和过氧化氢酶（CAT）的蛋白表达水平。
HF 组肥胖增加，但无脂肪细胞肥大和合并症。与 C 组相比，HF 和 HFS 组心脏 MDA 和羰基化蛋白水平升高。氧化和抗氧化蛋白水平在各组之间没有差异。
HF 和 HFS 饮食干预分别在存在和不存在肥胖的情况下促进了心脏氧化应激。然而，这一过程既不是由促氧化剂 AT1 和 Nox2 介导的，也不是由抗氧化酶的定量减少介导的。
