Postgraduate Program in Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Postgraduate Program in Nutrition and Health, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Cell Physiol Biochem. 2023 Aug 16;57(4):264-278. doi: 10.33594/000000642.
BACKGROUND/AIMS: Obesity resistance is associated with the complex interaction of stringent and environmental factors that confer the ability to resist mass gain and body fat deposition, even when eating high-calorie diets. Considering that there are numerous gaps in the literature on the metabolic processes that explain Obesity resistance, specifically in relation to oxidative stress, the purpose of the study was to investigate whether obesity-resistant (OR) rats develop elevated reactive oxygen species in cardiac tissue.
Wistar rats were initially randomized into two groups: a standard diet (SD) and a high-fat diet (HFD) group. The SD and HFD groups were further divided into control (C), OR, and obese prone (OP) subgroups based on body weight. This criterion consisted of organizing the animals in each group in ascending order according to body weight (BW), and the cutoff point was identified in the animals by terciles: 1) lower BW; 2) intermediate BW; and 3) higher BW. Rats were sacrificed on the 14th week, and serum and organs were collected. Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined.
BW showed a significant difference between the standard diet and high-fat diet groups in the 4th week of the experimental protocol, characterizing obesity. In the 4th week, after the characterization of Obesity resistance, there was a significant difference in BW between groups C, OP, and OR. The OP and OR groups showed a significant increase in caloric intake in relation to the C group. The OP group showed a significant increase in final BW, retroperitoneal fat pad mass, sum of corporal fat deposits and reactive oxygen species, in relation to groups C and OR. The area under the glycemic curve, insulin resistance index and basal glucose were elevated in the OP group in relation to the C. OP also promoted an increase in HOMA-IR when compared with C. OR rats showed a non-significant increase in insulin and HOMA-IR in OR vs. C (p = ~0.1), but no significant differences were observed between OP vs. OR for these parameters, suggesting that both groups suffered from decreased metabolic health. Total cardiac mass, left ventricular cross-sectional area, and cholesterol levels were significantly elevated in the OP and OR groups compared with the C group.
A high-fat diet induces cardiac damage in obesity-resistant rodents with reduction in metabolic health.
背景/目的：肥胖抵抗与严格和环境因素的复杂相互作用有关，这些因素赋予了抵抗体重增加和体脂肪沉积的能力，即使在食用高热量饮食时也是如此。考虑到关于解释肥胖抵抗的代谢过程的文献中有许多空白，特别是与氧化应激有关，本研究的目的是调查肥胖抵抗（OR）大鼠的心脏组织中是否会产生升高的活性氧。
Wistar 大鼠最初被随机分为两组：标准饮食（SD）组和高脂肪饮食（HFD）组。SD 和 HFD 组进一步根据体重分为对照组（C）、OR 组和肥胖易感性（OP）亚组。该标准包括根据体重对每组动物进行升序排列，临界点通过三分位数确定：1）较低体重；2）中等体重；3）较高体重。大鼠在第 14 周被处死，收集血清和器官。评估营养状况、食物谱、组织学分析、合并症和心血管特征。
在实验方案的第 4 周，标准饮食组和高脂肪饮食组之间的体重出现显著差异，表明肥胖。在第 4 周，肥胖抵抗特征确定后，C、OP 和 OR 组之间的体重出现显著差异。OP 和 OR 组的热量摄入与 C 组相比显著增加。与 C 和 OR 组相比，OP 组的最终体重、腹膜后脂肪垫质量、体脂肪沉积总和和活性氧显著增加。OP 组的血糖曲线下面积、胰岛素抵抗指数和基础血糖升高与 C 相比。与 C 相比，OP 还增加了 HOMA-IR。OR 大鼠的胰岛素和 HOMA-IR 在 OR 与 C 之间呈非显著增加（p = ~0.1），但 OP 与 OR 之间在这些参数上没有观察到显著差异，这表明两组代谢健康状况均下降。与 C 组相比，OP 和 OR 组的总心脏质量、左心室横截面积和胆固醇水平均显著升高。
高脂肪饮食可导致肥胖抵抗的啮齿动物心脏损伤，并降低代谢健康。
