目的 探讨大黄素改善KKAy糖尿病小鼠脂肪组织胰岛素敏感性及降血糖的作用机制.方法 将清洁级(SPF) KKAy小鼠20只按血糖值随机分为模型组、大黄素治疗组,按50 mg/( kg·d)剂量灌胃,并选10只C57 BL/6J小鼠为正常对照组,连续灌胃给药8周.8周后测定血清空腹血糖(FBG)、空腹胰岛素(Fins)并计算胰岛素敏感指数(ISI)、甘油三酯(TG)、总胆固醇(TC)及过氧化物酶体增殖物激活受体omRNA(PPAR-αmRNA)和过氧化物酶体增殖物激活受体γmRNA( PPAR-γmRNA)在脂肪组织的表达水平.结果 与正常对照组比较,模型组FBG、TG、TC明显升高,ISI明显降低,脂肪组织PPAR-αmRNA及PPAR-γmRNA的丰度表达明显降低(P＜0.05)；与模型组比较治疗组FBG、TG、TC明显降低,ISI明显升高,脂肪组织PPAR-αmRNA及PPAR-γmRNA的丰度表达明显升高(P＜0.05).结论 大黄素可以上调KKAy糖尿病小鼠脂肪组织PPAR-αmRNA及PPAR-γmRNA的表达,降低血糖、血脂并改善胰岛素敏感性.%Objective To discuss the effect of emodin for improving insulin sensitivity in lipid tissue and its mechanism of reducing plasma glucose in KKAy mice with diabetes. Methods SPF KKAy mice ( n = 20) were divided into model group and emodin group [ 50 mg/( kg· d) intragastrically giving] according to the value of blood glucose, and other 10 C57BL/6J mice were assigned as control group. After 8 weeks the levels of fasting blood glucose (FBG) and fasting insulin ( FINS) were detected, the insulin sensitivity index (ISI) was calculated, and triglyceride ( TG) , total cholesterol ( TC) , and the expressions of peroxisome proliferator activated receptor-α ( PPAR-amRNA) and peroxisome prliferator activated receptor-γ(PPAR-γmRNA) were determined. Results Compared with normal group, in model group the levels of FBG, TG and TC increased significantly, ISI decreased significantly and the expressions of PPAR-amRNA and PPAR-γmRNA decreased significantly (P <0.05). Compared with model group, in emodin group the levels of FBG, TG and TC decreased significantly, ISI increased significantly and the expressions of PPAR-amRNA and PPAR-^mRNA increased significantly (P<0.05). Conclusion Emodin can up-regulate the expressions of PPAR-αmRNA and PPAR-γ mRNA in lipid tissue, reduce plasma glucose and blood fat, and improve insulin sensitivity in KKAy mice with diabetes.
展开▼
