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目的:利用高脂饲料复制肥胖与肥胖抵抗型非酒精性脂肪肝SD大鼠模型。方法:体质量100±10g的雄性SD大鼠140只,按照体重随机抽取120只用于模型建立,喂食高脂、高能饲料。连续8周后,将体质量大于正常对照组平均体质量+1.96倍标准差的模型大鼠作为肥胖型非酒精性脂肪肝组(NO组),体质量小于正常对照组平均体质量+1.0倍标准差的作为肥胖抵抗型非酒精性脂肪肝组(NOR组)。8周内动态观察大鼠的一般情况、体质量变化,8周末每组随机取8只处死,比较血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、胆固醇(TC)、甘油三脂(TG)水平变化及肝指数、脂体比,观察肝脏形态学改变。剩余20只作为正常对照组,喂食普通饲料。结果:NO与NOR组大鼠体重增长差距逐渐增大,至8w末,NO组体重显著高于NOR组及正常对照组(P<0.01),脂肪重量和脂体比均显著升高,NO组脂肪重量显著高于NOR组(P<0.05,0.01),但脂体比间未见显著差异;NO与NOR组TG、ALT显著升高(P<0.05),其中NO组大鼠血清TG、TC显著高于NOR组(P<0.05);两组肝重量和肝指数均显著升高,NO组肝重量显著高于NOR组(P<0.05,0.01),但肝指数间未见显著差异,两组肝细胞内均弥散大量脂肪空泡。结论:利用高脂饲料成功建立肥胖与肥胖抵抗型非酒精性脂肪肝SD大鼠模型,与人类发病特征相似,为肥胖与非酒精性脂肪的研究提供更有针对性的动物模型。
OBJECTIVE: To copy obese and obesity resistant non-alcoholic fatty liver (SD) rat model by high-fat diet. METHODS: One hundred and fourteen male Sprague Dawley rats weighing 100 ± 10g were randomly selected according to body weight to establish a model and fed with high fat and high energy feed. After continuous 8 weeks, the body weight of the model group with the body mass greater than the normal body mass of 1.96 times the standard body weight of the normal control group was regarded as the obese non-alcoholic fatty liver group (NO group), the body weight was less than 1.0 times the average body weight of the normal control group Standard deviation as obesity resistant non-alcoholic fatty liver disease group (NOR group). Eight weeks later, the rats were sacrificed and 8 rats were sacrificed at random. The levels of serum ALT, AST, TC, TG ) Level changes and liver index, lipid ratio, observed liver morphological changes. The remaining 20 as a normal control group, fed normal feed. Results: The difference of body weight gain between NO group and NOR group increased gradually. At the end of 8th week, the body weight of NO group was significantly higher than that of NOR group and normal control group (P <0.01) Fat weight was significantly higher than NOR group (P <0.05,0.01), but there was no significant difference between the lipid ratio; NO and NOR group TG, ALT increased significantly (P <0.05), NO group rats serum TG, TC (P <0.05). The liver weight and liver index of the two groups were significantly increased. The liver weight of the NO group was significantly higher than that of the NOR group (P <0.05, 0.01), but there was no significant difference between the two indexes Group of hepatocytes dispersed a large number of fat vacuoles. Conclusion: The successful establishment of obese and obesity-resistant non-alcoholic fatty liver model rats with high-fat diet has similar characteristics with human pathogenesis and provides a more targeted animal model for the study of obesity and non-alcoholic fat.