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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C57BL/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αmRNA(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 investigate the mechanism of emodin in improving insulin sensitivity and hypoglycemia in adipose tissue of KKAy diabetic mice. Methods Twenty mice with clean-grade (KF) KKAy mice were randomly divided into model group and emodin-treated group. The mice were orally gavaged with 50 mg / (kg.d), and 10 C57BL / 6J mice were selected as normal Control group, continuous oral administration of 8 weeks. After 8 weeks, serum fasting blood glucose (FBG), fasting insulin (Fins) and insulin sensitivity index (ISI), triglyceride (TG), total cholesterol (TC) and peroxisome proliferator activated receptor αmRNA PPAR-αmRNA) and peroxisome proliferator activated receptorγmRNA (PPAR-γmRNA) in adipose tissue. Results Compared with the normal control group, FBG, TG and TC in the model group were significantly increased, ISI was significantly decreased, and the abundance of PPAR-αmRNA and PPAR-γmRNA in adipose tissue was significantly decreased (P <0.05). Compared with the model group, FBG (P <0.05). The levels of PPAR-α mRNA and PPAR-γ mRNA in adipose tissue were significantly increased (P <0.05). Conclusion Emodin can up-regulate the expression of PPAR-αmRNA and PPAR-γmRNA in adipose tissue of KKAy diabetic mice, reduce blood glucose, blood lipid and improve insulin sensitivity.