Objective To discuss the mechanism of Yiqi Yangyin formula on regulating the disorder of liver glucose metabolism in type2 diabetes model rats. Methods Healthy male SD rats were randomly divided into normal group(group 1, 10 rats) and model group(45 rats). The normal group were given basic diet; the model group was given high-fat and high-sugar diet. At the 6th week of experiment, the model group were intraperitoneal injection with 30 mg/kg STZ, and then randomly divided into model group (group 2), TCM group(group 3) and western medicine group(group 4), 10 rats in each group. Group 3 were given the Yiqi Yangyin formula[4. 80 g/(kg·d)], and group 4 were given pioglitazone hydrochloride [1. 35 g/(kg·d)], the normal group and model group were given the same amount of distilled water, the treatment was lasted for two weeks. The indicators associated with the deficiency of both qi and yin, hepatic insulin resistance and liver glucose metabolism on type 2 diabetes wer observed. Results Compared with group 1, FPG, Fins, IRI, blood cGMP, liver PEPCK, G-6-P, GSK-3 of group 2 were significantly increased (P<0. 01);the cAMP, cAMP/cGMP and Na+-K+-ATPase in blood, the liver InsR,IRS-2 and glycogen content was significantly decreased (P<0. 05, P<0. 01). Compared with the group 2, the FPG, IRI in blood and PEPCK, GSK-3 in liver of group 3 and group 4 were significantly decreased (P<0. 05 or P<0. 01);the Fins, cGMP in blood and G-6-P in liver of group 3 was decreased, but the level of cAMP , cAMP / cGMP and Na+-K+-ATPase in blood, IRS-1, glycogen in liver were sig-nificantly increased (P<0. 05, P<0. 01); Compared with group 4, the cGMP was decreased, but the cAMP, cAMP/cGMP and Na+ -K+ -ATPase were increased ( P<0. 05, P<0. 01 ) of the group3. Conclusion The Yiqi Yangyin formula can regulate the disorder of liver glucose metabolism in type 2 diabetes model rats, the mechanism is to regulate both the insulin receptors and the enzymes related to glucose metabolism.%目的：探查益气养阴方对气阴两虚2型糖尿病型大鼠肝脏糖代谢紊乱的调节机制。方法雄性SD大鼠随机分为正常组10只和造模组45只。其中正常组给予基础饲料喂养；模型组给予高脂高糖饲料喂养。第6周,造模组大鼠给予一次性腹腔注射30 mg/kg链脲佐菌素,并于实验第6周末,选择空腹血糖≥11.1mmol/L的造模组大鼠随机分为模型组、中药组、西药组,每组10只；中药组给予益气养阴方[4.80 g/(kg·d)],西药组给予盐酸吡格列酮[1.35 g/(kg·d)],正常组和模型组分别以等量蒸馏水灌胃,连续给药两周。给药后,检测2型糖尿病气阴两虚证、肝脏胰岛素抵抗、肝脏糖代谢相关指标。结果与正常组相比,模型组大鼠血中血糖( fasting plasma glucose,FPG)、血清胰岛素(fasting serum insulin,Fins)、胰岛素抵抗指数(insulin resistance index,IRI)、环磷酸鸟苷( cyclic guanosine monophosphate, cGMP )、肝脏磷酸烯醇式丙酮酸羧激酶( phosphoenolpyruvate carboxykinase,PEPCK)、葡萄糖-6-磷酸酶( G-6-P)、糖原合成酶激酶-3( glycogen synthasc kinase-3, GSK-3)均明显升高(P<0.01)；大鼠血中环磷酸腺苷(Cyclic Adenosine monophosphate,cAMP)、cAMP/cGMP和红细胞膜 Na+-K+-ATP 酶(Na+-K+-ATPase),肝脏胰岛素受体(Insulin receptor, InsR)和胰岛素受体底物2(insulin receptor substrate,IRS-2)、肝糖原含量均明显下降(P<0.05或P<0.01)；与模型组相比,中药组和西药组大鼠FPG、IRI、肝脏PEPCK、GSK-3明显降低( P<0.05或P<0.01),并且中药组血中Fins、cGMP、G-6-P下降,cAMP、cAMP/cGMP、红细胞膜Na+-K+-ATPase、IRS-1和肝糖原含量均明显上升(P<0.05或P<0.01)。与西药组相比,中药组大鼠血中cGMP降低, cAMP、cAMP/cGMP和红细胞膜Na+-K+-ATPase均升高(P<0.01)。结论益气养阴方对2型糖尿病气阴两虚证大鼠的肝脏糖代谢有改善作用,其机制与胰岛素受体和糖代谢相关酶的调节有关。
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