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Serum TNF-α GTH and MDA of high-fat diet-induced obesity and obesity resistant rats

机译:高脂饮食诱导的肥胖和肥胖抵抗大鼠的血清TNF-αGTH和MDA

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摘要

Objective: Mechanism of high fat diet-induced obesity is analyzed and serum tumor necrosis factor, malondialdehyde and glutathione levels of obesity resistant rats are effectively analyzed. Methods: 120 male SD rats were grouped into obesity group and control group, each group with 60 rats. Obese rats were fed with high fat diet, while control rats were fed with ordinary fodder. After six months of feeding, growth degree of two groups of rats is observed , and the rats are divided into obesity group and obesity resistant group based on extent of growth. Then glutathione, tumor necrosis factor-α and MDA content in bat serum are detected with enzyme-linked immunosorbent assay. Results: The content of tumor necrosis factor α in obese rats and obesity resistant rats is far higher than that in control group (P < 0.05), there exists no statistical significance (P > 0.05) in tumor necrosis factor α in obesity group and obesity resistant group, glutathione level of obesity group rats and obesity resistant group rats is significantly increased (P < 0.05) compared with that of control group, and also serum MDA level of the two groups has statistical significance compared with that of normal control group (P < 0.05). Conclusion: Among rats fed with high fat diet, in comparison with weight of obesity resistant rats and control group rats, there is no statistically significant difference, (P > 0.05). However, high fat diet will impact mechanisms in vivo in rats, which then induces oxidative stress response and inflammatory response in rats.
机译:目的:分析高脂饮食诱发肥胖的机理,并有效分析肥胖抵抗大鼠的血清肿瘤坏死因子,丙二醛和谷胱甘肽水平。方法:将120只雄性SD大鼠分为肥胖组和对照组,每组60只。肥胖大鼠饲喂高脂饮食,而对照大鼠饲喂普通饲料。喂食六个月后,观察两组大鼠的生长程度,根据生长程度将其分为肥胖组和肥胖抵抗组。用酶联免疫吸附法检测蝙蝠血清中的谷胱甘肽,肿瘤坏死因子-α和MDA含量。结果:肥胖大鼠和肥胖抵抗力大鼠中的肿瘤坏死因子α含量远高于对照组(P <0.05),肥胖组和肥胖患者中的肿瘤坏死因子α无统计学意义(P> 0.05)抵抗组,肥胖组大鼠和肥胖抵抗组大鼠的谷胱甘肽水平明显高于对照组(P <0.05),并且两组血清MDA水平与正常对照组相比也具有统计学意义(P <0.05)。结论:在高脂饮食喂养的大鼠中,与肥胖抵抗性大鼠和对照组大鼠的体重相比,差异无统计学意义(P> 0.05)。但是,高脂饮食会影响大鼠体内的机制,进而诱发大鼠氧化应激反应和炎症反应。

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