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目的观察二甲双胍对2型糖尿病大鼠脂肪组织中腺苷酸活化蛋白激酶α2(AMPKα2)表达及对氧化应激水平的影响,探讨其改善血糖、氧化应激及胰岛素抵抗的可能机制。方法 32只雄性SD大鼠随机分为正常对照组(NC,n=12)、糖尿病模型组(DM,n=10)、二甲双胍治疗组(MT,n=10);后两组高脂饮食1个月后腹腔注射链脲佐菌素(STZ)30 mg/kg制备2型糖尿病大鼠模型。造模成功后,MT组给予二甲双胍50 mg/(kg.d)灌胃,NC组、DM组给予同剂量0.5%羟甲基纤维素钠溶液。测定大鼠治疗前后的体质量,并检测各组空腹血糖(FBG)、空腹胰岛素(FINS)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、β-N-乙酰氨基葡萄糖苷酶(NAG)、髓过氧化物酶(MPO)、丙二醛(MDA)、单胺氧化酶(MAO)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)水平,计算大鼠脂体比、胰岛素敏感指数(ISI)。同时以半定量RT-PCR检测脂肪组织AMPKα2 mRNA的表达。结果与DM组比较,MT组脂肪组织AMPKα2 mRNA的表达及血清GSH、SOD、ISI、HDL增高,FINS、FBG、NAG、MDA、MPO、MAO、TC、TG、LDL降低,差异均有统计学意义(P<0.05)。结论二甲双胍调节2型糖尿病大鼠,糖脂代谢,改善胰岛素敏感性及氧化应激可能与脂肪组织AMPKα2的表达增加有关。
Objective To observe the effect of metformin on the expression of AMPKα2 and the level of oxidative stress in adipose tissue of type 2 diabetic rats and to explore its possible mechanism of improving blood glucose, oxidative stress and insulin resistance. Methods Thirty-two male SD rats were randomly divided into normal control group (NC, n = 12), diabetic model group (DM, n = 10) and metformin treatment group (MT, n = 10) The model rats with type 2 diabetes were prepared by intraperitoneal injection of streptozotocin (STZ) 30 mg / kg after one month. After successful modeling, MT group was given 50 mg / (kg · d) of metformin. The rats in NC group and DM group were given 0.5% sodium carboxymethyl cellulose solution. The body weight of rats before and after treatment was measured and the levels of fasting blood glucose (FBG), fasting insulin (FINS), superoxide dismutase (SOD), glutathione (GSH), β-N-acetylglucosamine NAG, MPO, MDA, MAO, TC, TG, HDL, low density lipoprotein Protein (LDL) levels were calculated. Lipid ratio and insulin sensitivity index (ISI) were calculated. Semi-quantitative RT-PCR was used to detect the expression of AMPKα2 mRNA in adipose tissue. Results Compared with DM group, the expression of AMPKα2 mRNA in adipose tissue and the levels of serum GSH, SOD, ISI and HDL in adipose tissue of MT group were increased and the levels of FINS, FBG, NAG, MDA, MPO, MAO, TC, TG and LDL were decreased (P <0.05). Conclusion Metformin modulates glucose metabolism, improves insulin sensitivity and oxidative stress in type 2 diabetic rats, which may be related to the increased expression of AMPKα2 in adipose tissue.