Influência de diferentes tipos de dietas hipercalóricas sobre parâmetros metabólicos, inflamatórios e de estresse oxidativo

• Autor(a) principal: Kobi, Jéssika Butcovsky Botto Sarter
• Data de Publicação: 2019
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/11238
• topic: Obesity; Hypercaloric diets; Inflammation; Oxidative stress; Obesidade; Dietas hipercalóricas; Inflamação; Estresse oxidativo; Nutrição

Introduction: Obesity is considered a worldwide epidemic and a serious public health problem of the 21 century. The consumption of hypercaloric diets can be the main contributor to the current epidemic of overweight, obesity and comorbidities in all over the world. Excess adipose tissue affects the mitochondrial metabolism, contributing to the development of oxidative stress. Another important aspect is the relationship between obesity and metabolic diseases with chronic state of inflammation. Objective: Investigate the influence of three types of hyper caloric diets on metabolic parameters, inflammatory and oxidative stress in experimental model. Material and Methods: This study was approved by the Ethical Commission on the Use of Animals of the Federal University of Espirito Santo (08/2016). Thirty- day-old male Wistar rats (n = 40) were randomized into four groups: control (C), high- sucrose (HS), high-fat (HF) and high-fat with sucrose (HFS) for 20 weeks. Nutritional, metabolic, hormonal and biochemical profiles as well as the histological analyzes of adipose and hepatic tissues were performed. Inflammation was assessed by serum levels of inflammatory markers such as interleukin 6 (IL-6) and adiponectin. Activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in serum and biomarkers of oxidative stress in serum and homogenates of visceral and epididymal adipose tissue (malondialdehyde (MDA) and carbonylated proteins) were determined. Data were expressed as mean ± standard error of the mean or median ± interquartile range, and were submitted to analysis of variance (ANOVA) one-way for independent samples (diet) and two-way (diet and time) for the repeated measures model, complemented with the Tukey's and/or Kruskal-Wallis post hoc test. The level of significance was 5%. Results: HF promoted obesity with a significant increase in final body weight (HF: 658 ± 43 vs. C: 525 ± 17 and HS: 543 ± 16, p<0.05), body fat (HF: 71 ± 7 vs. C: 44 ± 2 and HS: 44 ± 4, p<0.05) and adiposity index (HF: 11 ± 1 vs. C: 8.4 ± 0.3 and HS: 7.9 ± 0.5, p<0.05) in relation to C and HS. The comorbidities associated with obesity were the glucose intolerance visualized by higher area under the glycemic curve (AUC) in the HF and HFS groups than C (C = 1234 ± 65 vs. HF = 1521 ± 57 and HFS = 1460 ± 45, p <0.05). In addition, hypertension was visualized in all experimental groups when compared to C. In relation to the hormonal and biochemical parameters, there was no significant difference between the experimental groups. The experimental groups showed increased fat droplets deposition in the hepatic tissue when compared to group C, although the adipocyte areas were similar. The concentrations of oxidative stress biomarkers (MDA and carbonylated proteins) in serum and visceral and epididymal adipose tissue were similar between the groups. In addition, there was no significant difference for the activity of the antioxidant enzymes SOD and CAT in the serum. Inflammatory markers (IL-6 and adiponectin) also showed similar results between groups. Conclusion: The hyperlipid model was effective in triggering obesity and comorbidities associated, but all experimental models of hypercaloric diets were unable to promote oxidative stress and inflammation.