摘要
目的观察水通道蛋白7在自发糖尿病模型OLETF大鼠不同糖尿病病程的皮下和附睾脂肪组织中的表达,探讨AQP7与肥胖糖尿病的关系。方法 OLETF大鼠组分为未治疗组(OLETF组)及盐酸二甲双胍治疗组(OLETF/M组)。观察不同周龄时大鼠的体重、血清甘油三酯、胆固醇、甘油、葡萄糖耐量实验血糖与胰岛素以及皮下和附睾脂肪组织AQP7 mRNA和AQP7蛋白含量的变化。Rea1-time PCR测定AQP7 mRNA水平,Western blotting测定AQP7蛋白含量。结果随周龄增加,肥胖、血脂紊乱加重,胰岛素抵抗明显,血糖增高。OLETF组皮下脂肪AQP7 mRNA及蛋白表达为逐渐上调趋势,附睾脂肪AQP7 mRNA及蛋白表达先上调后下调,皮下脂肪AQP7 mRNA及蛋白表达上调幅度大于附睾脂肪AQP7。盐酸二甲双胍改善了OLETF/M组大鼠的脂代谢和糖代谢紊乱,且OLETF/M组皮下及附睾脂肪组织AQP7 mRNA及蛋白表达上调幅度均低于OLETF组。结论皮下及附睾脂肪组织的AQP7在肥胖和糖尿病的发生发展中起一定作用。
Objective To observe subcutaneous adipose tissue(SAT) and epididymal adipose tissue (EAT)aquaporin 7 (AQPT) mRNA and protein expression in the spontaneous type 2 diabetes animal model OLETF rats in different stages of diabetes and explore the role of AQP7 in obesity and diabetes development. Methods OLETF rats were divided into no treatment group (OLETF groUp) and metformin treatment group (OLETF/M group). At the different weeks, body weights were obtained, biochemical items were measured , including serum triglyceride, cholesterol, glycerol, glucose and insulin with oral glucose tolerance test (OGTT). The SAT and EAT were obtained for measuring the AQP7 mRNA expression by real time PCR and AQP7 protein expression by Western blotting. Results The degrees of obesity, dyslipidemia, insulin resistance and glucose of OLETF rats were significantly and gradually increased along with week-age increment (all P^0. 05 or d0. 01). SAT AQP7 mRNA and protein expressios were gradually increased with aging. EAT AQP7 mRNA and protein expressions were increased at the age of 18 weeks but decreased at the age of 28 weeks. Expressions of AQP7 mRNA and protein were higher in SAT than in EAT. Metformin can improve disorders of lipid metabolism and glucose metabolism in the OLETF/M rats, and SAT and EAT AQP7 mRNA and protein expressions were lower in OLETF/M group than in OLETF group. Conclusions SAT and EAT AQP7 may play an important role in the development of obesity and diabetes.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2011年第3期216-220,共5页
Chinese Journal of Diabetes
基金
教育部归国基金[教外司留2006331]