原钒酸钠对2型糖尿病大鼠骨骼肌GLUT4mRNA表达的影响

 目的 观察原钒酸钠(sodium orthovanadate)对2型糖尿病大鼠骨骼肌葡萄糖转运蛋白4(GLUT4)mRNA表达的影响。方法 用高脂饲料灌胃正常大鼠10 d,引起肥胖,再用四氧嘧啶(120mg·kg^-1)腹腔注射,建立2型糖尿病大鼠模型。筛选空腹血糖值大于16.7 mmol·L^-1的大鼠,随机分成5组:原钒酸钠大剂量组(9 mg·kg^-1·d^-1)、原钒酸钠中剂量组(3 mg·kg^-1·d^-1)、原钒酸钠小剂量组(1 mg·kg^-1·d^-1)、糖尿病模型组、苯乙双胍组(75 mg·kg^-1·d^-1)。连续用药7d,用快速血糖仪测空腹血糖值。用胰岛素放免试剂盒测血清胰岛素值。用骨骼肌GLUT4原位杂交试剂盒检测骨骼肌GLUT4 mRNA的表达。结果①2型糖尿病大鼠经原钒酸钠灌胃给药后,空腹血糖值与模型组相比有明显的降低(P<0.05);②用药组大鼠血清胰岛素值与模型组相比无显著差异;③用药组大鼠的骨骼肌GLUT4 mRNA表达量与模型组相比均有明显增多。结论 原钒酸钠对2型糖尿病大鼠有明显的降糖作用,对血清胰岛素的分泌无明显影响,对2型糖尿病大鼠骨骼肌GLUT4 mRNA的表达有促进作用。     

葛根素对大鼠胰岛素刺激下骨骼肌细胞膜GLUT4蛋白含量的影响

目的 :了解葛根素对糖尿病胰岛素抵抗状态是否有改善作用 ,并探讨这种作用是否通过影响大鼠骨骼肌细胞膜GLUT4蛋白含量而实现。方法 :制备胰岛素抵抗大鼠模型。将动物分为 3组 :正常对照组 ;胰岛素抵抗模型组 ;胰岛素抵抗模型 +葛根素治疗组。第 3组大鼠腹腔注射葛根素 100mg·kg^-1·d^-1,治疗 4周。用Westernblot方法检测骨骼肌细胞膜表面GLUT4蛋白表达。结果 :胰岛素抵抗模型组大鼠骨骼肌细胞膜GLUT4蛋白表达显著减少 ,与正常对照组相比 ,减少约 31% ;用葛根素注射液治疗后 ,细胞膜GLUT4蛋白表达明显上调 ,约 1.18倍。结论 :葛根素可能通过降糖、改善高胰岛素血症 ,从而影响细胞内胰岛素信号传导 ,使GLUT4转位至细胞膜增加 ,其在膜上的含量也增加 ,发挥快速转运葡萄糖的作用。     

Amelioration of insulin resistance using the additive effect of ferulic acid and resveratrol on vesicle trafficking for skeletal muscle glucose metabolism

Dysregulation of vesicle trafficking in muscle is one of the factors responsible for the pathogenesis of insulin resistance (IR). Ferulic acid (FER) and resveratrol (RSV) are known to have hypoglycemic property. In this study, differentiated L6 myotubes were induced with palmitate as a model of IR. Chemical ablation of muscle vesicles was used to investigate how FER and RSV influence glucose utilization. Results showed that both FER and RSV elicit glucose uptake and promote glycogen synthesis in insulin‐resistant muscle cells. Mechanistic studies further showed that FER markedly enhances the transferrin receptor‐containing endosomal compartment activities via phosphoinositide 3‐kinase (PI3K)/atypical protein kinase C‐dependent pathway, while RSV facilitates glucose transporter storage vesicles (GSV) trafficking via an exercise‐like effect of conventional protein kinase C/5′‐adenosine monophosphate‐activated protein kinase (AMPK) modulation. Therefore, these two phenolic compounds promoted glucose transport through two separate routes, and they had an additive effect on the increase of glucose uptake in insulin‐resistant muscle cells. These findings provide a basis for the understanding of the antidiabetic potential of RSV and FER combination.     

Ginsenoside Rg1 promotes glucose uptake through activated AMPK pathway in insulin-resistant muscle cells

Ginsenoside Rg1, a protopanaxatriols saponin, is one of the major active constituents from Panax ginseng and possesses various biological activities. A recent study reported that insulin resistance in skeletal muscle is a major contributor to the development of type 2 diabetes mellitus (T2DM). We examined the effects of ginsenoside Rg1 on glucose uptake and the associated molecular mechanisms of the glucose transport system in insulin-resistant muscle cells. The insulin resistance of the muscle cell was induced by treatment of differentiated C2C12 cells with chronic insulin. The results showed that chronic treatment of insulin resulted in reduced glucose uptake in the muscle cells. The treatment of ginsenoside Rg1 significantly enhanced glucose uptake in the differentiated muscle cells and the relative abundance of GLUT4 through the adenosine-monophosphate-activated protein kinase pathway. These results suggest that ginsenoside Rg1 improved the insulin resistance in C2C12 muscle cells, which might be useful for prevention of T2DM and metabolic syndromes.     

Cardamonin stimulates glucose uptake through translocation of glucose transporter-4 in L6 myotubes

Glucose transporter-4 (GLUT4) is a transmembrane protein that plays a major role in insulin-mediated glucose transport in muscle and adipocytes. For glucose transport to occur, the GLUT4 protein needs to be translocated from the intracellular pool to the plasma membrane, and certain compounds may enhance this process. The present study investigated the promotion of glucose uptake in differentiated L6 myotubes by cardamonin, isolated from Alpinia katsumadai. Cardamonin increased translocation of GLUT4 to the plasma membrane in L6 cells, but did not activate protein kinase C ζ/λ, Akt, or AMP-activated protein-kinase, all of which are known to regulate GLUT4 translocation. The glucose-uptake-promoting activity of cardamonin was not lowered by treatment with a phosphatidylinositol 3'-kinase inhibitor. These results suggest that cardamonin is a promising active compound for maintaining glucose homeostasis, and that it acts via an unknown mechanism that does not involve activation of the downstream insulin signal and AMP-activated protein kinase.     

绿原酸对高脂饲喂大鼠骨骼肌糖代谢的影响

目的 研究绿原酸对高脂饲喂SD大鼠骨骼肌糖代谢的调节机制。方法 40只雄性SD大鼠随机分成5组:对照组、模型组,低、高剂量(20、90 mg/kg)绿原酸组,罗格列酮(阳性对照)组,其中对照组饲喂普通饲料,其余各组大鼠饲喂高脂饲料。给药12周后处死大鼠,取骨骼肌,用实时荧光定量-PCR方法测定骨骼肌糖代谢过程中相关基因蛋白激酶B(PKB,又名Akt)、磷脂酰肌醇-3激酶(PI3K)、胰岛素受体底物-1(IRS-1)、葡萄糖转运蛋白4(GLUT-4)、蛋白激酶A(PKA)、AMP依赖的蛋白激酶(AMPK-α2)、过氧化物酶体增殖物激活受体(PPARα、PPARβ、PPARγ)的表达。结果 与对照组比较,模型组大鼠骨骼肌中GLUT-4、AMPK-α2和PPARβ mRNA表达量显著下降(P< 0.05、0.01);与模型组相比,绿原酸干预能提高糖代谢途径中相关基因的表达,其中绿原酸高剂量组Akt、PI3K、IRS-1、GLUT-4、PKA、AMPK-α2、PPARα、PPARβ mRNA的表达量显著上调(P< 0.05、0.01)。结论 高剂量绿原酸能显著减缓高脂饲喂SD大鼠体质量增加,并通过调节PI3K/Akt途径、AMPK途径和胰岛素敏感性,改善骨骼肌中糖代谢。     

Effect of some hypoglycemic glycans on glucose uptake and glucose metabolism by inverted intestinal fragments

Polysaccharides which lowered blood glucose concentration in vivo, were examined for their effects on glucose uptake and glucose oxidation by inverted intestinal fragments of rats. The examined polysaccharides exhibited dose-dependent stimulations of glucose oxidation (CO₂ release) between 75 and 300 μg/ml incubation mixture. The effects increased to maximal values, as compared to the control at external glucose concentrations of 0.06-0.25 mM (depending on the glycan), after which inhibitory trends were observed. No effect on the rate of glucose uptake could be observed.     

吴茱萸次碱对胰岛素抵抗骨骼肌细胞炎症因子表达的影响

探讨吴茱萸次碱（rutecarpine,Rut）对胰岛素抵抗原代骨骼肌细胞（insulin resistant primary skeletal muscle cells,IR-PSMC）中炎症因子的影响。培养原代大鼠骨骼肌细胞,显微镜下观察细胞形态学变化,MTT法观察Rut对原代骨骼肌细胞增殖的影响。用棕榈酸（PA）诱导建立IR-PSMC细胞,氧化酶-过氧化物酶（GOD-POD）法检测培养基中葡萄糖浓度,并检测Rut对IR-PSMC细胞中炎症因子IL-1,IL-6,TNF-α的影响。原代骨骼肌细胞培养7 d后,细胞长满培养皿,Rut在0~180.0 μmol·L^-1,对原代骨骼肌细胞增殖无明显影响。用0.6 mmol·L^-1PA培养24 h可建立IR-PSMC细胞,Rut在20~180 μmol·L^-1抑制IR-PSMC细胞中IL-1,IL-6,TNF-α生成,且具良好的量效关系。Rut可能通过抗炎来促进IR-PSMC细胞葡萄糖吸收及改善胰岛素抵抗。     

The effects of essential oil of Mentha x villosa on skeletal muscle of the toad

The effects of the essential oil of Mentha x villosa (EOMV) was investigated in saponin-permeabilized fibres and in intact sartorius muscle of the toad. In intact muscle EOMV at concentrations from 1 to 100 μg/mL blocked the contraction induced by high (80 mM ) potassium and induced potentiation of caffeine-induced muscle contraction. From 1 to 6 mg/mL EOMV elicited contraction in both depolarized (by 110 mM K⁺) and non-depolarized (4 mM K⁺) muscle fibres. This contraction was blocked by procaine. At 3 mg/mL EOMV depolarized the normal resting potential from −80.77 to −71.21 mV, but did not alter the transmembrane potential in the presence of 60 mM K⁺. EOMV (1 mg/mL) induced contraction of saponin-permeabilized muscle fibres with an intact sarcoplasmic reticulum (SR). These data suggest that EOMV: (i) induces muscle contraction by releasing Ca²⁺ from SR; (ii) impairs the excitation–contraction coupling at a step before Ca²⁺ release from the SR. © 1997 John Wiley & Sons, Ltd.     

丹蛭降糖胶囊对糖尿病胰岛素抵抗大鼠骨骼肌葡萄糖转运体Ⅳ基因表达的影响

目的：观察丹蛭降糖胶囊对糖尿病胰岛素抵抗模型大鼠骨骼肌葡萄糖转运体Ⅳ（GLUT4）基因表达的影响，以初步明确其作用靶点。方法：雄性Wistar大鼠随机分为空白组、模型组、中药低剂量组、中药高剂量组、西药组、中西药合用组。空白组喂以普通饲料，模型组与各治疗组注射小剂量链脲佐菌素并喂以高热量饲料，常规测定各组大鼠治疗前后的体重、空腹血糖和治疗后各组大鼠的空腹血脂、血清胰岛素水平，计算胰岛素敏感性指数，用Northern印迹和杂交法测定骨骼肌GLUT4基因的表达。结果：丹蛭降糖胶囊能有效地减轻模型大鼠体重，能明显降低大鼠的空腹血糖和胰岛素水平，改善脂代谢紊乱状况，能增加胰岛素抵抗（IR）大鼠骨骼肌中GLUT4 mRNA的表达，从而改善了外周组织的胰岛素敏感性。结论：丹蛭降糖胶囊对2型糖尿病大鼠 IR有显著的改善作用，提示其机制可能与增加IR大鼠骨骼肌中GLUT4 mRNA的表达有关。     

电针调控骨骼肌胰岛素受体底物-1磷酸化改善胰岛素抵抗的机制

目的:观察电针对2型糖尿病大鼠骨骼肌胰岛素受体底物-1(IRS-1)磷酸化水平的影响,从而探讨电针治疗2型糖尿病的可能机制.方法:采用2型糖尿病肥胖大鼠作为研究对象.将成模后的14只ZDF大鼠随机分为模型组、电针组,每组7只;另将7只ZL大鼠设为空白组.干预4周,检测空腹血糖(FBG),并以Western Blot法检...     

Coriolus versicolor aqueous extract ameliorates insulin resistance with PI3K/Akt and p38 MAPK signaling pathways involved in diabetic skeletal muscle

Patients with type 2 diabetes mellitus (T2DM) are usually with poor immunity and easier to suffer from cancer and microbial infections. Herein, we report an efficient anti‐diabetic medicinal mushroom, Coriolus versicolor (CV). This study aimed to investigate the anti‐diabetic and anti‐insulin‐resistance effects of CV aqueous extract in myoblasts (L6 cells) and skeletal muscle of T2DM rat. Our results showed that CV extract treatment significantly reduced blood glucose levels of T2DM rats, whereas CV extract increased glucose consumption in insulin resistant L6 cells. Besides, the translocation and expression of glucose transporter 4 were enhanced by CV extract, which indicated that CV extract was effective in diabetic skeletal muscle. Moreover, CV extract treatments resulted in remarkable anti‐insulin‐resistance effects, which was reflected by the change of gene and protein expression levels in PI3K/Akt and p38 MAPK pathways. PI3K inhibitor, LY29004, and p38 MAPK inhibitor, SB203580 confirmed it further. In conclusion, our results demonstrated that the CV extract exhibited anti‐diabetic and anti‐insulin‐resistance effects in diabetic skeletal muscle, and the effects were mediated by PI3K/Akt and p38 MAPK pathways. These findings are remarkable when considering the use of commercially available CV by diabetic patients who also suffer from cancer or microbial infections.     

银杏叶提取物增强糖尿病大鼠模型膈肌摄取葡萄糖能力的作用研究

目的:观察银杏叶提取物(GbE)对糖尿病大鼠模型膈肌葡萄糖摄取率和葡萄糖转运体4(GLUT4)mRNA表达水平的影响.方法:40只雄性SD大鼠随机分为正常对照组10只,造模组30只.应用高糖高脂饮食加小剂量链脲佐菌素诱发糖尿病大鼠模型.随机选取造模成功大鼠20只均分成2组:糖尿病组、GbE治疗组.GbE治疗组按8 mg·kg~(-1)·d~(-1)剂量腹腔注射GbE,持续8周.检测各组大鼠空腹血糖和胰岛素水平,膈肌组织葡萄糖摄取率和CLUT4 mRNA水平,并观察其超微结构的变化.结果:与正常对照组比较,糖尿病组大鼠空腹血糖和胰岛素升高(P<0.01);膈肌葡萄糖摄取率和GLUT4 mR-NA水平下降(P<0.05,P<0.01);电镜下主要表现为膈肌线粒体扩张,嵴变短,空泡化.GbE治疗组L述变化明显减轻.结论:GbE可部分纠正糖尿病大鼠模型高血糖、高胰岛素状态,并减轻膈肌损伤,其作用与增强膈肌GLUT4基因表达,促进膈肌对葡萄糖的摄取和利用有关.     

消肿止痛膏对腓肠肌损伤大鼠MyoD mRNA与蛋白表达的影响

目的基于微小RNA表达机制,探讨消肿止痛膏对大鼠骨骼肌损伤后重塑和修复的影响。方法通过钝挫伤模型的方法建立大鼠腓肠肌损伤模型,观察消肿止痛膏对大鼠损伤后4、7、14、21天定量PCR检测腓肠肌MyoD mRNA与蛋白表达水平,探讨消肿止痛膏对大鼠腓肠肌钝挫伤模型的肌肉重塑与修复的作用机制。结果治疗组MyoD mRNA表达与蛋白表达水平在造模后14天、21天均显著高于空白组与模型组(P<0.05),进一步证实消肿止痛膏在骨骼肌重塑及修复过程中所起的重要作用。MyoD在损伤后7天上升,其后表达一直维持在较高水平,至损伤后21天仍可以表达出较高水平。与模型组相比较,其表达的高峰期在14天左右,其后则基本回归到一般状态。结论大鼠腓肠肌损伤后,在自然修复过程中,生肌调节因子的表达水平呈现上升-回落的趋势,其中损伤后7～14天,为其表达的高峰期。MyoD的表达水平呈现上升趋势,即使至损伤后21天,其表达仍未见明显下降趋势,可见消肿止痛软膏可以促进MyoD的表达。消肿止痛软膏可以促进MyoD的表达,可以调节骨骼肌的再生修复,提示消肿止痛膏可以通过基因调控,发挥对骨骼肌损伤后的再生修复作用。     

Effect of ginsenosides Rg3 and Re on glucose transport in mature 3T3-L1 adipocytes

Ginsenosides, the active component of Panax ginseng, have been shown to evidence a variety of biological activities associated with hyperglycemia, obesity and type 2 diabetes mellitus. This study evaluated the effects of the ginsenosides, Rg3 and Re, on glucose uptake and the glucose transport system in mature 3T3‐L1 cells. The results demonstrated that the glucose uptake of ginsenosides Rg3 and Re at concentrations of 1–10 µM significantly increased by approximately ～10% and ～12%, respectively. Furthermore, the glucose transporter 4 (GLUT4) mRNA expression of ginsenosides Rg3 and Re at 10 µM was increased by approximately ～1.73 and 1.43 fold, respectively. It was further confirmed in a series of experiments that ginsenosides Rg3 and Re stimulated the mRNA expression of insulin receptor substrate (IRS‐1) and the expression of phosphatidylinositol 3‐kinase (PI3K)‐110α protein, which is involved in downstream events in the insulin signaling pathway. These findings demonstrate that ginsenosides Rg3 and Re may stimulate glucose uptake via the PI3K pathways involving IRS‐1. Further, our results suggest that both of these ginsenosides might prove useful as effective antidiabetic and antihyperglycemic agents. Copyright © 2010 John Wiley & Sons, Ltd.     

近5年推拿修复骨骼肌损伤的作用机制研究进展

牵拉伤、钝挫伤以及失神经支配损伤等常见损伤都可以造成骨骼肌的损害,若修复不完全则容易形成瘢痕,影响肌肉功能。骨骼肌损伤在中医学中属于“筋伤”的范畴,推拿作为传统治疗筋伤病的重要方式之一,在治疗骨骼肌损伤中有广泛的应用。近些年逐渐开展了关于推拿修复骨骼肌损伤机制的研究,通过文献总结,发现推拿可通过磷脂酰肌醇激酶（PI3K）、丝裂原活化蛋白激酶（MAPK）、Notch、Wnt及过氧化物酶体增殖因子活化受体（PPAR）信号通路对骨骼肌的修复产生影响。推拿以肌卫星细胞为重点,通过促进如成肌调节因子（MRFs）、胰岛素样生长因子-1（IGF-1）、碱性成纤维细胞生长因子（bFGF）等正向调节因子的表达,抑制如转化生长因子-β（TGF-β）、生长分化因子-8（GDF-8）、结缔组织生长因子（CTGF）等负向调节因子的表达,以及下调肿瘤坏死因子-α（TNF-α）及白细胞介素-6（IL-6）等炎性因子的浓度,来发挥促进肌纤维重塑、防止细胞外基质过度沉积、减轻炎症反应以及减缓骨骼肌纤维化的作用。除此之外,推拿还可以通过促进细胞合理自噬、修复细胞膜、调节氧化应激及脂肪代谢等反应促进组织修复。本文聚焦于推拿修复骨骼肌损伤的机制,以期为进一步研究提供参考。     

津力达颗粒对骨骼肌线粒体生物发生和胰岛素敏感性的影响

目的探讨中成药津力达颗粒对骨骼肌线粒体生物发生和胰岛素敏感性的影响。方法随机将雄性SD大鼠分为正常饲养组12只、高脂饲养组24只,6周后每组选取6只行高胰岛素-正葡萄糖钳夹试验,鉴定造模成功后,分别测定体重、胰岛素抵抗指数(HOMA-IR)、腹腔注射葡萄糖耐量实验(IPGTT)、葡萄糖输注率(GIR)等。余造模成功高脂喂养的18只大鼠进一步分为模型组、吡格列酮干预组、津力达颗粒干预组,继续喂养8周,分别测定体重、血脂、IPGTT、GIR等,并检测骨骼肌组织中Toll样受体2(TLR2)蛋白,以及线粒体生物发生指标过氧化物酶体增殖物激活受体γ共激活因子α(PGC1α)、线粒体融合蛋白2(MFN2)、核呼吸因子1(NRF-1)和胰岛素信号通路磷脂酰肌醇3激酶(PI3K)、磷酸化蛋白激酶B(P-AKT)、葡萄糖转运蛋白4(GLUT4)等蛋白的表达水平。结果①喂养6周后:与正常组相比,模型组体重、HOMA-IR均显著升高,IPGTT各时点血糖显著升高,GIR明显下降,差异均有统计学意义(P<0.05)。②喂养14周后:与模型组相比,吡格列酮干预组和津力达颗粒干预组大鼠体重及血脂水平明显下降,IPGTT各时点血糖显著下降,GIR显著升高,差异均有统计学意义(P<0.05)。③喂养14周后:与模型组相比,津力达颗粒干预组和吡格列酮干预组上调了线粒体生物发生指标PGC1α、MFN2、NRF-1以及胰岛素信号通路PI3K、P-AKT、GLUT4等蛋白表达水平,并且下调了骨骼肌组织中TLR2蛋白的表达,差异有统计学意义(P<0.05)。结论津力达颗粒与吡格列酮类似,可能通过促进骨骼肌线粒体生物发生而改善胰岛素敏感性。     

糖肾胶囊对FFR模型骨骼肌及脂肪组织GLUT4mRNA表达的影响

目的探讨糖肾胶囊对高果糖餐大鼠(fructose-fed rats,FFR)模型胰岛素抵抗(insolin resistance IR)改善的机制。方法20只清洁级6周龄雄性SD大鼠随机等分为4组,即正常对照组以标准餐喂养,后三组(模型对照组、糖肾胶囊组、文迪雅组)以高果糖餐喂养4周即可成模。成模后三组分别投喂生理盐水和糖肾胶囊(800mg·kg~(-1)·d~(-1))、文迪雅(2 mg·kg(-1)·d(-1))4周。取各组大鼠的骨骼肌和脂肪组织,分别用RT-PCR和荧光定量PCR技术对两种组织的GLUT4mRNA进行定性定量分析。结果糖肾胶囊能减少骨骼肌和增加脂肪组织的GLUT4mRNA表达(P＜0．05)。结论糖肾胶囊可能是通过影响骨骼肌和脂肪组织GLUT4mRNA表达改善胰鸟素抵抗的。     

双清平化方对代谢综合征大鼠骨骼肌自噬通路蛋白表达的影响

目的 观察双清平化方对代谢综合征大鼠Lee''s指数、血糖、血脂及骨骼肌哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)、自噬效应蛋白1(Beclin1)、微管相关蛋白1轻链3(microtubule-associated protein1 light chain 3,LC3)蛋白表达的影响,探讨其改善糖脂代谢的作用机制。方法 大鼠给予高脂饲料加10%果糖水溶液喂养,并联合应用N-硝基-L-精氨酸甲酯(N-nitro-L-arginine methyl ester,L-NAME)及链脲佐菌素(streptozotocin,STZ)诱导代谢综合征模型。代谢综合征大鼠给予双清平化方或二甲双胍干预8周,实验前后定期测量大鼠体质量、体长、腹围、血压、糖耐量、糖化血红蛋白(glycated hemoglobin,GHb)、胰岛素(insulin,INS)、总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)、高密度脂蛋白胆固醇(high-density lipoprotein cholesterol,HDL-C),计算葡萄糖曲线下面积(OGTT-AUC)和胰岛素抵抗指数(HOMA-IR);采用苏木素-伊红(HE)染色观察骨骼肌组织病理形态学变化;采用Masson染色观察骨骼肌纤维形态变化;采用免疫组化法检测骨骼肌组织中LC3蛋白表达;采用Western blotting检测骨骼肌组织中mTOR、Beclin1和LC3蛋白表达。结果 与对照组比较,模型组大鼠空腹血糖(fasting blood glucose,FBG)、餐后2 h血糖(2 h postprandial glucose,PG2h)、OGTT-AUC、HOMA-IR、INS、GHb、TC、TG及LDL-C水平均显著升高(P<0.01),HDL-C水平显著降低(P<0.01);骨骼肌组织中mTOR蛋白表达显著上调(P<0.01),Beclin1、LC3蛋白表达显著下调(P<0.01)。与模型组比较,双清平化方组FBG、PG2h、OGTT-AUC、HOMA-IR、INS、GHb、TC、TG及LDL-C水平均显著降低(P<0.05、0.01),HDL-C水平显著升高(P<0.01);骨骼肌组织中mTOR蛋白表达水平显著上调(P<0.01),Beclin1和LC3蛋白表达显著下调(P<0.01)。结论 双清平化方可以改善代谢综合征大鼠胰岛素抵抗,改善糖脂代谢水平,抑制骨骼肌病理变化,其作用机制可能与调节骨骼肌自噬,激活骨骼肌组织自噬通路中mTOR、Beclin1、LC3蛋白表达有关。