高脂饮食诱导下的肥胖和肥胖抵抗大鼠细胞形态及瘦素、AMPK表达变化的研究  

Research on the Variance of Tissue Morphology,Leptin and AMPK between Obesity and Obesity-resistant Rats under High-fat Diet Inducement

作　　者：郭光[1] 田荣[2] 曲卉[3] 李杰[4] 

机构地区：[1]西北工业大学体育部,陕西西安710072 [2]西北工业大学明德学院体育教研室,陕西西安710124 [3]中国人民武装警察部队工程学院,陕西西安710086 [4]中国人民武装警察部队技术学院,陕西西安710086

出　　处：《北京体育大学学报》2011年第3期67-70,共4页Journal of Beijing Sport University

摘　　要：目的:旨在发现肥胖和肥胖抵抗大鼠体脂、细胞形态、瘦素、AMPK发生的变化,研究肥胖抵抗发生的机制,为预防人类肥胖,调整不合理的饮食结构,降低疾病的发生提供一定的理论依据。方法:选取3-4周龄离乳SD雄性大鼠90只,适应性喂养1周后,随机分为2组,正常对照组(NS)9只、高脂饮食诱导组(HS)81只,通过13周的高脂饮食诱导催肥,选出肥胖大鼠8只,肥胖抵抗大鼠8只,进行体重,体脂,细胞形态学、瘦素与AMPK活性测试。结果:1)高脂饮食喂养导致大鼠肥胖、体脂增加,同时出现肥胖和肥胖抵抗两种现象;2)肥胖抵抗大鼠体脂百分比显著低于肥胖组大鼠,与正常对照组大鼠相比有升高趋势;3)在相同面积视野下,肥胖组与肥胖抵抗组大鼠肠系膜脂肪细胞数量显著低于正常对照组,而脂肪厚度显著增加;同时肥胖抵抗组大鼠肠系膜脂肪细胞数量较肥胖组稍高,而脂肪厚度较肥胖组大鼠下降;4)肥胖组与肥胖抵抗组大鼠瘦素水平在喂养过程中出现增加趋势且显著高于正常对照组;5)肥胖组大鼠AMPK活性在喂养过程中出现下降趋势,肥胖抵抗组大鼠出现升高趋势且显著高于肥胖组大鼠。结论:经高脂喂养的大鼠出现肥胖抵抗现象可能与其瘦素水平提高,从而促进AMPK活性提高有关。Objective：This article＇s aim was to discover the variance of body weight,body fat,tissue morphology,leptin and activity of AMPK between obesity and obesity-resistant rats and research the mechanism of DIO-R,provide some theoretical basis for prevention of human obesity,the readjustment of irrational diet,reduce the incidence of disease.Methods： 90 male weanling SD rats aged 3-4 week,adaptive feeding for one week were randomly divided into two groups,9 in normal control group（NS）,81 in high-fat diet-induced group（HS）,through the 13-week high-fat diet-induced fatten to elect eight obese rats and eight obesity-resistant rats to measure body weight,body fat,cell morphology test,test leptin in blood and activity of AMPK.Results：1）Rats which fed by high-fat diet result in weight increased and occurred obesity and obesity-resistance.2）The obesity-resistant rats＇ weight were notably lower than obese rats and normal rats,the percentage of body fat content was also significantly lower than obese rats in obesity-resistant rats,also showed increasing trend comparing with the normal rats.3）In the same proportion,the mesenteric fat cells in obesity-resistance and obese ones were notably lower than in normal ones,the fat thickness increased significantly.The obesity-resistance rats had lower mesenteric fat cells and fat thickness than obese ones,but had no notable changes.4）The leptin values of obesity-resistance and obese rats appeared to have an increasing trend,the values also significantly higher than normal ones.5）The decreasing trend of activity of AMPK appeared in obese rats,in contrast,the increasing trend appeared in obesity-resistance rats and significantly higher than obese ones.Conclusions：The result of obesity-resistance was leaded by increasing of activity of AMPK by leptin increasing.

关 键 词：高脂饮食 肥胖 肥胖抵抗 瘦素 AMPK活性 

分 类 号：R589.2[医药卫生—内分泌]