摘要
目的建立饮食诱导非酒精性脂肪肝病(NAFLD)合并高血糖动物模型并观察其特点。方法将64只SD大鼠随机分为2组。正常对照组(用普通饲料饲喂)32只,高糖高脂组(饲以高糖高脂饲料)32只,连续喂养12个月。于实验第3月末、第6月末、第9月末、第12月末观察动物体重、内脏脂肪重量;比较血液中有关血脂、血糖、炎症介质等方面的生化指标以及组织病理学观察。结果与正常对照组相比,各阶段高糖高脂组大鼠体重、内脏脂肪重量明显增加;血清ALT、FFA、LPS、TNFα、FPG、FINS和HOMA-IR的水平都升高,其差异有统计学意义;而HOMA-β以第六个月出现代偿性增强后进行性衰退。病理组织学显示肝脏发生严重的脂变、脂肪肝进而发生肝炎、纤维化及肝硬化;随时间进展胰岛逐渐萎缩并伴有炎性浸润;脂肪细胞逐渐增大并伴有炎性浸润。结论高糖高脂饮食可建立大鼠NAFLD合并高血糖动物模型,该模型可在NAFLD和相关的糖尿病研究中发挥作用。
Objective To establish an animal of diet induced non-alcoholic fatty liver disease（NAFLD） and hyperglycemia,and to investigate its features.Methods 64 rats were randomly divided into 2 groups.The control group（fed with normal diet） 32,high glucose and high fat group（fed with high sugar and high fat diet） 32,continuous feeding of 12 months.on the 3month、6months、9 months、12 month of the experiments,we observe animal weight,visceral fat weight;Comparing relevant in the blood lipid levels,blood sugar,inflammatory mediators aspects of biochemical indicators and observed histopathologically.Results Compared with the normal control group,weight and visceral fat weightof the animals of high glucose and high fat groups increased obviously;the level of ALT,FFA,LPS,TNF,FPG,FINS and HOMA-IR of hig sucrose and high fat groups of every phases were higer,but the level of HOMA-beta of 6H group rats first showed the compensatory increase,then progressive decrease in sequence.The pathological and histological display liver produces serious steatosis,fatty liver and hepatitis,fibrosis and cirrhosis occurs;Over time progress islet gradually atrophic,accompanied by inflammatory infiltrate;Fat cells gradually increasing and accompanied by inflammatory infiltrate.Conclusion High sugar and fat diet can establish rats models of NAFLD and hyperglycemia,this model can be play important role in NAFLD and related diabetes research.
出处
《中国比较医学杂志》
CAS
2011年第7期22-27,79,共7页
Chinese Journal of Comparative Medicine
基金
山西省自然科学基金资助项目(NO.2008011073-1)
关键词
糖毒性
脂毒性
非酒精性脂肪性肝病
2型糖尿病
胰岛素抵抗
Lipotoxicity
glucotoxicity
Nonalcoholic fatty liver disease
Type Ⅱdiabetes
Insulin resistance
