机构地区:[1]广州中医药大学附属中山中医院儿科,广东中山528400
出 处:《临床医学》2013年第12期87-90,共4页Clinical Medicine
基 金:广东省中山市医疗卫生科技计划项目(2011-3A-078)
摘 要:目的本研究通过建立新生大鼠低血糖模型,然后再以此为基础,诱发非酒精性脂肪性肝病(NAFLD),通过比较不同组间病变程度、胰岛素抵抗强弱、肝功能等指标的差异,了解新生大鼠低血糖和NAFLD易感性之间的关系,为了解NAFLD的发生机制和寻找有效的防治措施提供实验依据。方法购SPF级成熟Wistar雌性大鼠20只和雄性大鼠10只,合笼交配,从所生仔鼠中每窝随机抽取0—1只,总共12只作为正常血糖+正常饮食组;然后将相同母鼠所生3只新生大鼠,随机分入正常血糖+高脂饮食组、低血糖+正常饮食组、低血糖+高脂饮食组各12只,在第20周末处死,测血清空腹血糖(FBG)、血清空腹胰岛素(FINS)、脂肪酸、总胆固醇(TCH)、三酰甘油(TG)、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)等指标。肝组织石蜡切片染色判断肝脂变和炎症活动情况。结果20周末大鼠胰岛素抵抗指数(IRI)、脂肪酸、TG、ALT、AST在正常血糖+高脂饮食组、低血糖+正常饮食组中明显高于正常血糖+正常饮食组,低血糖+高脂饮食组中明显高于正常血糖+高脂饮食组、低血糖+正常饮食组;TCH在正常血糖+高脂饮食组、低血糖+高脂饮食组中明显高于正常血糖+正常饮食组、低血糖+正常饮食组。病理学指标检测中,肝脂变指数及炎症指数在正常血糖+高脂饮食组、低血糖+正常饮食组中明显高于正常血糖+正常饮食组,低血糖+高脂饮食组中明显高于正常血糖+高脂饮食组、低血糖+正常饮食组。结论新生大鼠低血糖所导致的代谢紊乱会导致NAFLD的发生。Objective To investigate the relationship between neonatal rat hypoglycemia and susceptibility to non-alcoholic fatty liver disease(NAFLD). The neonatal rat model of hypoglycemia was estblished, on this basis, nonalcoholic fatty liver dis- ease was induced. Then, the difference of the severity of the disease, insulin resistance strength and liver function index of all groups were recorded. It would provide the experimental basis for the occurrence and clarify the mechanism of NAFLD and 'find out the effective prevention and control measures. Methods Thirty SPF mature Wistar rats (female 20, male 10 ) were ob- tained. Then let them mated. From the birth of each litter were randomly selected 0 - 1 only. A total of 12 rats will be selected as the normal blood glucose + normal diet group. Three neonatal rats which were born by the same rats, were divided into normal glucose + high fat diet group, normal diet group + hypoglycemia, hypoglycemia + high fat diet group. Each group had 12 .rats. These rats were sacrificed at the end of 20th week. Before these rats were put to death, the changes of fasting blood + glucose, fasting serum insulin ( FINS), fatty acid, total cholesterol ( TCH ), triglyceride ( TG), alanine aminotransferase ( ALT), and aspartate aminotransferase (AST)were obtained and evaluated. Hepatic injury was assessed by the histopathology( H + E) ac- cording to the scoring system proposed by Brunt. Results After 20 weeks, insulin resistance index (IRI) , fatty acid, triglyceride (TG) , alanine aminotransferase ( ALT), aspartate aminotransferase ( AST), which were in the rats of the euglycemia + high fat diet group and normal diet ~ hypoglycemia group, were significantly higher than those in euglycemia + normal diet group, and those in hypoglycemia + high fat diet group were significantly higher than those in euglycemia + high fat diet group and hypoglyce- mia + normal diet group. Total cholesterol (TCH) in the euglycemia + high f
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