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目的:探讨左归降糖益肾方对高脂饮食转基因2型糖尿病MKR鼠糖脂代谢及炎症反应的影响。方法:用左归降糖益肾方干预治疗高脂饲料喂养的转基因2型糖尿病MKR鼠,采用电化学法测定空腹血糖浓度,采用全自动生化分析仪检测血脂和超敏C反应蛋白(hs-CRP),采用酶联接免疫吸附剂测定(ELISA)检测血清胰岛素与肿瘤坏死因子-α(TNF-α)水平。结果:高脂饲料喂养的MKR小鼠空腹血糖高于MKR组,但无统计学意义;血清胰岛素,血总胆固醇(TCHO),血低密度脂蛋白胆固醇(LDL-C),血高密度脂蛋白胆固醇(HDL-C),LDL-C/HDL-C,血清hs-CRP和TNF-α水平高于MKR组(P<0.01),而甘油三酯(TG)下降,低于MKR组(P<0.01)。经左归降糖益肾方或文迪雅干预治疗后,高脂饮食MKR小鼠血糖、血清胰岛素,TG,LDL-C/HDL-C,血清hs-CRP和TNF-α水平显著下降(P<0.05,P<0.01);左归降糖益肾方组TCHO,LDL-C下降(P<0.05),HDL-C上升(P<0.05),而文迪雅对照组TCHO,LDL-C下降和HDL-C上升无统计学意义。结论:左归降糖益肾方能减轻高脂饮食加重的MKR鼠的胰岛素抵抗,增强外周组织对胰岛素的敏感性,调节高脂饮食MKR鼠糖脂代谢,减少炎症因子的产生。
Objective: To investigate the influence of Zuoguijiang TangYishen Recipe on glucose and lipid metabolism and inflammation in transgenic mice with type 2 diabetes mellitus with high-fat diet. Methods: The Zuogong Jiangtangshen decoction was used to treat the transgenic type 2 diabetes mellitus (MKR) rats fed with high-fat diet. The fasting blood glucose concentration was determined by electrochemical method. The levels of serum lipid and high sensitivity C-reactive protein (hs- CRP). The levels of serum insulin and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). Results: The fasting blood glucose of MKR mice fed with high fat diet was higher than that of MKR mice, but there was no significant difference between the two groups. Serum insulin, total cholesterol (TCHO), LDL-C and blood high density lipoprotein The level of serum HDL-C, HDL-C, serum hs-CRP and TNF-α in serum of MKR group were significantly higher than that of MKR group (P <0.01) 0.01). The serum glucose, serum insulin, TG, LDL-C / HDL-C, serum hs-CRP and TNF-α levels in MKR mice were decreased significantly (P <0.05, P <0.01). The TCHO and LDL-C in Zuogui Tang and Yishen Recipe decreased (P <0.05) and HDL-C increased And HDL-C increased without statistical significance. Conclusion: Zuogui Jiangtang Yishen can relieve insulin resistance of MKR rats exacerbated by high-fat diet, enhance the sensitivity of peripheral tissues to insulin, and regulate the metabolism of glucose and lipids in high-fat diet MKR mice and reduce the production of inflammatory factors.