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OBJECTIVE: The study suggests that obesity is the combined result of multiple genetic factors and environmental impact. In modern society, rich in high-energy, fat, sugary foods and drinks everywhere, high-fat high-sugar diet has become the main diet, and is considered one of the main environmental cause human obesity. This high-fat high-sugar diet on human physiological system, more and more people pay attention. Most view the body from high-fat high-sugar diet, the more energy, the more obese, and accompanied by the reduction of glucose tolerance. More than 20 years ago, Ruderman proposed the concept of the metabolically obese normal weight (Metabolically Obese, Normal-Weight, MONW), pointed out that this population is not overweight, but atherogenic metabolic abnormalities, so far unknown etiology. Our aim is to explore the high-fat high-sugar diet experimental normal-weight metabolically obese rat model of oxidative stress and chronic inflammation of the state. Method: 1. Animal experiments: male SD rats 60 (weight 60g-70g, 4 weeks old) were fed for four weeks adaptability. Feeding period, the temperature and humidity suitable for day and night 12 hours, the rats with normal diet and water ad libitum. After the end of the adaptive feeding, the rats were randomly divided into: (1) normal diet group, 20 rats were given a normal diet feeding, (2) high-fat high-sugar diet group, 40 rats were given a high-fat high-sugar forage . Weekly weighing the body weight of rats. At 29 weeks, the inner canthus venous blood was collected and centrifuged supernatant serum, -80 ℃ to save the serum under test. A total of six rats died in the course of the experiment, and finally into the normal diet rats 18 statistics, 36 high-fat high-sugar diet rats. Inflammatory cytokines determination: ELISA (Enzyme-Linked Immunosorbent assay, ELISA) kit measured serum high sensitivity C-reactive protein (high sensitive C-reactive protein, hs-CRP), monocyte chemotactic factor -1 (monocyte chemoattractant protein-1, MCP-1) and plasminogen activator inhibitor -1 (plasminogen activator inhibitor-1, PAI-1) levels. Oxidative stress parameters were measured: measured serum malondialdehyde (malondialdehyde, MDA), superoxide dismutase (superoxide dismutase, SOD) levels in order to observe the high fat and sugar diet rats in vivo oxidative stress conditions. Results: 1. Rats with high fat and sugar diet group and normal diet group weight gain during the experiment (189.19 ± 59.38g vs 174.94 ± 80.20g, t = -0.738, P = 0.464) and final body weight (469.83 ± 13.62g vs 447.89 ± 22.77g, t = -0.875, P = 0.386) was not statistically different. High fat and sugar diet serum hs-CRP (1503.63 ± 895.63ng/ml vs 896.99 ± 506.72ng/ml, t = -3.173, P = 0.003), MCP-1 (212.86 ± 60.31pg/ml vs162 .00 ± 38.63pg/ml, t = -3.252, P = 0.002), PAI-1 (10.31 ± 2.33ng/ml vs7.64 ± 1.71ng/ml, t = -4.312, P = 0.000) were significantly higher in the control group, a statistically significant difference. Rat serum MDA level of the high-fat and high-sugar diet group was significantly higher than the normal diet group (6.37 ± 1.08nmol / L vs 5.68 ± 0.75nmol / L, and t = -2.425, P = 0.019), SOD levels were significantly lower than the ordinary feed group (334.40 ± 61.35U/ml vs 383.98 ± 52.74U/ml, t = 2.927, P = 0.005), a statistically significant difference. Conclusion: In this study, the use of high-fat high-sugar diet successfully established a normal weight metabolically obese SD rat model. This rat model presents a similar model with obesity, chronic inflammation of the low activity and oxidative stress.
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