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作 者:武革[1] 陈玉华[1] 杨璐[1] 胡桂芳[1] 吴美芬[1]
机构地区:[1]广东医学院附属医院内分泌科,广东湛江524001
出 处:《广东医学》2012年第23期3519-3522,共4页Guangdong Medical Journal
基 金:广东省医学科研基金资助项目(编号:A2004469)
摘 要:目的探讨持续高脂饲养加链脲佐霉素诱导2型糖尿病伴非酒精性脂肪性肝病(NAFLD)大鼠解偶联蛋白-2(UCP2)在肝脏中的表达及意义。方法 30只雄性SD大鼠随机分为正常对照组、NAFLD组及T2DM伴NAFLD组。分别给予正常饮食和持续高脂饮食喂养,于8、16周末T2DM伴NAFLD组加链脲佐霉素(STZ)30mg/kg腹腔注射。观察各组大鼠肝脏脂肪变性情况,用免疫组织化学染色观察肝脏UCP2蛋白表达,以半定量逆转录-聚合酶链反应(RT-PCR)检测肝脏UCP2 mRNA的表达,同步取血检测各组大鼠血糖、胰岛素、肝功能、血脂水平。结果随喂养时间延长NAFLD组及T2DM伴NAFLD组大鼠出现肝脏广泛水样变性和不同程度脂肪变性及血糖、胰岛素、肝酶、血脂水平升高,与正常对照组比较差异有统计学意义(P=0.002);NAFLD组及T2DM伴NAFLD组肝脏UCP2蛋白表达及mRNA表达均明显升高,与正常对照组比较差异有统计学意义(P<0.001);T2DM伴NAFLD组较单纯NAFLD组UCP2表达增加更为明显(P<0.001)。结论持续高脂喂养加小剂量STZ诱导的T2DM伴NAFLD组大鼠较单纯NAFLD组大鼠肝脏UCP2蛋白及mRNA表达增高显著,伴肝脏脂肪变性及炎症反应更严重,可能是T2DM伴NAFLD发生的因素之一。Objective To investigate the expressions of UCP2 in liver of rats with long - term fat - enriched fed and lower dose of streptozoein - induced type 2 diabetes mellitus (T2DM) with nonalcoholic fatty liver disease (NAFLD). Methods Thirty rats were randomly divided into normal groups, the NAFLD group, T2DM with NAFLD group. The subjects in normal control group were raised by standard animal feeds, while in NAFLD group by highly fat - enriched diet for 8 and 16 week, and in T2DM with NAFLD with plus lower dose of streptozocin (30 mg/kg). The livers were examined pathologically. The expressions of UCP2 in the liver were assessed by immunohistochemistry and semi - quantitative RT - PCR. The blood glucose, liver function, lipoprotein, and insulin were recorded at the 8th and 16th week. Results With the feeding times extended, extensive hydropic degeneration and varied steatosis were detected in the rat livers in NAFLD and T2DM with NAFLD groups, so were the significant elevation of blood glucose, insulin, liver enzymes, and lipids (P =0. 002). There were also significant up - regulation of UCP2 protein and mRNA in both NAFLD and T2DM with NAFLD groups (P 〈0. 001 ), while it was significantly more prominent in T2DM with NAFLD group (P 〈0. 001 ). Conclusion The expression of UCP2 in rats with T2DM and NAFLD, which present severe hepatic steatosis and inflammation, is dramatically up -regulated, as compared with those with NAFLD alone.
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