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目的:探究津力达对高脂诱导的胰岛素抵抗Apo E-/-小鼠骨骼肌脂质转运酶类相关基因的表达变化。方法:8只雄性C57BL/6J小鼠设为正常组(NF);40只雄性Apo E-/-小鼠喂养16周后分为模型组(HF)、罗格列酮组(LGLT)、津力达低剂量组(JLDL)、津力达中剂量组(JLDM)、津力达高剂量组(JLDH),开始灌胃给药,连续8周。采用组织游离脂肪酸、BCA蛋白浓度法测定骨骼肌FFA含量;实时荧光定量反转录PCR(RT-PCR)和蛋白质印迹法(Western blot)测定小鼠骨骼肌脂肪酸转位酶(FAT/CD36)、肉毒碱棕榈酰基转移酶1(CPT1)、过氧化物酶体增殖物激活受体α(PPARα)mRNA和蛋白表达。结果:津力达能够不同程度降低小鼠的空腹血糖(FBG)、胆固醇(TC)、甘油三酯(TG)和游离脂肪酸(FFA);下调空腹胰岛素(FIns)水平,提高胰岛素敏感指数(ISI);津力达能够不同程度的上调小鼠CPT1,PPARαmRNA和蛋白表达,下调FAT/CD36的mRNA和蛋白水平。结论:津力达能够通过调节骨骼肌脂质转运酶类的表达变化,改善高脂诱导的Apo E-/-小鼠的胰岛素抵抗。
OBJECTIVE: To investigate the effect of Jinlida on the expression of lipase-related genes in skeletal muscle of insulin-resistant ApoE - / - mice induced by high fat diet. Methods: Eight male C57BL / 6J mice were assigned as normal group (NF). Forty male Apo E - / - mice were fed for 16 weeks and then divided into model group (HF), rosiglitazone group (LGLT) Low dose group (JLDL), middle dose group (JLDM), and high dose group (JLDH) of Jin Lida, started gavage for 8 weeks. The content of FFA in skeletal muscle was determined by the method of tissue free fatty acid and BCA protein concentration. The skeletal muscle fatty acid translocase (FAT / CD36) Carnitine Palmitoyl Transferase 1 (CPT1), Peroxisome Proliferator Activated Receptor α (PPARα) mRNA and Protein Expression. Results: Jinlida could decrease fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG) and free fatty acid (FFA), reduce FIns level and increase insulin sensitivity index ); Jinlida up-regulated the mRNA and protein expression of CPT1 and PPARα, and down-regulated the mRNA and protein levels of FAT / CD36 in mice. CONCLUSION: ZunLiDa can improve the insulin resistance of ApoE - / - mice induced by high fat by regulating the expression changes of lipase in skeletal muscle.