祛胰抵方对胰岛素抵抗3T3-L1脂肪细胞脂联素、瘦素及抵抗素表达的影响
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摘要
目的:观察祛胰抵方对胰岛素抵抗(insulin resistance,IR) 3T3-L1脂肪细胞脂联素、瘦素及抵抗素表达的影响,明确祛胰抵方治疗2型糖尿病(type 2 diabetes mellitus,T2DM)胰岛素抵抗的作用机制。方法:采用细胞培养技术,将3T3-L1前脂肪细胞诱导分化为成熟脂肪细胞,通过地塞米松与胰岛素共同诱导建立IR细胞模型。将脂肪细胞分为对照组、模型组、吡格列酮组、祛胰抵方高剂量组、祛胰抵方中剂量组和祛胰抵方低剂量组。以葡萄糖氧化酶法检测培养液中葡萄糖消耗量,酶联免疫吸附试验(ELISA)法检测脂联素、瘦素和抵抗素的分泌水平。结果:与对照组比较,模型组脂联素含有量降低,瘦素和抵抗素含量升高,差异均有统计学意义(P<0.05);与模型组比较,祛胰抵方高剂量组、祛胰抵方中剂量组、祛胰抵方低剂量组及吡格列酮组脂联素含量明显升高,瘦素、抵抗素含有量显著降低,差异均有统计学意义(P<0.05)。与祛胰抵方中剂量组比较,脂联素的含量高于祛胰抵方高剂量组、祛胰抵方低剂量组,祛胰抵方高剂量组抵抗素、瘦素含量低于吡格列酮组及祛胰抵方中剂量组、祛胰抵方低剂量组,差异均具有统计学意义(P<0.05)。结论:祛胰抵方可增加脂联素分泌,减少瘦素和抵抗素的分泌,从而改善IR。
Objective:To observe the influence of Formula for Removing Insulin on the expression of 3 T3-L1 adipocyte adiponectin and leptin and resistin,and clarify its mechanism in treating insulin resistance of type 2 diabetes mellitus(T2 DM).Methods:The adipocytes before 3 T3-L1 were induced to differentiate into mature adipocytes by cell culture technique.IR cell model was established by co-induction of dexamethasone and insulin.The adipocytes were divided into the control group,the model group,the pioglitazone group,the high-dose FRIR group,the medium-dose FRIR group and the low-dose FRIR group.Glucose consumption in culture medium was detected by glucose oxidase method,and the secretion levels of adiponectin,leptin and resistin were detected by enzyme-linked immunosorbent assay(ELISA).Results:Compared with the control group,the content of adiponectin in the model group decreased,while the content of leptin and resistin increased.And all the differences were statistically significant(P<0.05).Compared with the model group,the contents of adiponectin of the high-dose FRIR group,the medium-dose FRIR group the low-dose FRIR group,and the pioglitazone group increased significantly,while the contents of leptin and resistin decreased significantly,and all the differences were statistically significant(P<0.05).The content of adiponectin of the medium-dose FRIR group was higher than that of the high-dose FRIR group and that of the low-dose FRIR group.The resistin and leptin of the high-dose FRIR group were lower than those of the medium-dose FRIR group and those of the low-dose FRIR group,and all the differences were statistically significant(P<0.05).Conclusion:Formula for Removing Insulin Resistance can increase the secretion of adiponectin and reduce the secretion of leptin and resistin,thus improving IR.
Objective:To observe the influence of Formula for Removing Insulin on the expression of 3 T3-L1 adipocyte adiponectin and leptin and resistin,and clarify its mechanism in treating insulin resistance of type 2 diabetes mellitus(T2 DM).Methods:The adipocytes before 3 T3-L1 were induced to differentiate into mature adipocytes by cell culture technique.IR cell model was established by co-induction of dexamethasone and insulin.The adipocytes were divided into the control group,the model group,the pioglitazone group,the high-dose FRIR group,the medium-dose FRIR group and the low-dose FRIR group.Glucose consumption in culture medium was detected by glucose oxidase method,and the secretion levels of adiponectin,leptin and resistin were detected by enzyme-linked immunosorbent assay(ELISA).Results:Compared with the control group,the content of adiponectin in the model group decreased,while the content of leptin and resistin increased.And all the differences were statistically significant(P<0.05).Compared with the model group,the contents of adiponectin of the high-dose FRIR group,the medium-dose FRIR group the low-dose FRIR group,and the pioglitazone group increased significantly,while the contents of leptin and resistin decreased significantly,and all the differences were statistically significant(P<0.05).The content of adiponectin of the medium-dose FRIR group was higher than that of the high-dose FRIR group and that of the low-dose FRIR group.The resistin and leptin of the high-dose FRIR group were lower than those of the medium-dose FRIR group and those of the low-dose FRIR group,and all the differences were statistically significant(P<0.05).Conclusion:Formula for Removing Insulin Resistance can increase the secretion of adiponectin and reduce the secretion of leptin and resistin,thus improving IR.
引文
[1] 马中书,冯晓路,朱萍.代谢综合征与相关疾病的临床研究进展[J].中国全科医学,2015,18(17):1991-1995.
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[3] 张世卿,佟丽.胰岛素抵抗作用发生机制及实验模型的研究进展[J].中药新药与临床药理,2012,23(3):364-368.
[4] 王仁山,王晔华.胰岛素抵抗的成因[J].实用糖尿病杂志,2016,12(6):60-62.
[5] 朱冰,曲伸.瘦素调节糖代谢的机制研究进展[J].中国糖尿病杂志,2016,24(11):1040-1043.
[6] 任毅,左之才,万涛梅.抵抗素在胰岛素抵抗中的作用机制及其受体信号通路研究进展[J].生理学报,2016,68(1):65-74.
[7] 聂绪强,杨建文,史海霞,等.IR-3T3-L1脂肪胰岛素抵抗细胞的建立[J].南方医科大学学报,2015,35(1):103-108.
[8] 刘晓华,江湖,李海星,等.胰岛素诱导3T3-L1脂肪细胞胰岛素抵抗模型的建立[J].食品科学,2012,33(19):249-253.
[9] 谢利芳,许志华,郭凯霞.2型糖尿病胰岛素抵抗研究进展[J].科学技术与工程,2010,10(15):3664-3669,3672.
[10] 安平,王安平,母义明.脂联素与胰岛素抵抗研究进展[J].生物技术通讯,2017,28(3):360-365.
[11] 郭燕,蔡艳,白云霞,等.血清脂联素、胰岛素抵抗与代谢综合征的相关性研究[J].中国实用医药,2016,11(29):8-10.
[12] 任毅,左之才,万涛梅.抵抗素在胰岛素抵抗中的作用机制及其受体信号通路研究进展[J].生理学报,2016,68(1):65-74.
[13] 王春炅,张园,管又飞,等.瘦素在糖脂代谢中的调控作用[J].中国生物化学与分子生物学报,2009,25(10):896-902.
[14] 周婧婧,高玉敏,赵灵燕.瘦素及瘦素受体与糖尿病关系的研究进展[J].内蒙古医学杂志,2016,48(4):442-444.
[15] 黄彩华,陈俊钦,林建新,等.运动改善2型糖尿病胰岛素抵抗与血清脂联素和瘦素及其交互作用[J].中国体育科技,2011,47(4):100-105.
[16] 马建,姚秀明,赵娜,等.祛胰抵方对2型糖尿病胰岛素抵抗大鼠PI-3K的影响[J].中医药学报,2013,41(5):50-53.
[17] 马建,马晓静,杜丽坤,等.祛胰抵方对2型糖尿病胰岛素抵抗大鼠骨骼肌细胞膜葡萄糖转运蛋白4的影响[J].医学研究杂志,2013,42(9):58-60.
[18] 闫玲玲,马建.祛胰抵方对2型糖尿病IR的临床观察[J].中医药学报,2012,40(1):113-115.
[2] 李影,闫鹏,董平栓.胰岛素抵抗的分子学机制[J].医学综述,2014,20(17):3122-3124.
[3] 张世卿,佟丽.胰岛素抵抗作用发生机制及实验模型的研究进展[J].中药新药与临床药理,2012,23(3):364-368.
[4] 王仁山,王晔华.胰岛素抵抗的成因[J].实用糖尿病杂志,2016,12(6):60-62.
[5] 朱冰,曲伸.瘦素调节糖代谢的机制研究进展[J].中国糖尿病杂志,2016,24(11):1040-1043.
[6] 任毅,左之才,万涛梅.抵抗素在胰岛素抵抗中的作用机制及其受体信号通路研究进展[J].生理学报,2016,68(1):65-74.
[7] 聂绪强,杨建文,史海霞,等.IR-3T3-L1脂肪胰岛素抵抗细胞的建立[J].南方医科大学学报,2015,35(1):103-108.
[8] 刘晓华,江湖,李海星,等.胰岛素诱导3T3-L1脂肪细胞胰岛素抵抗模型的建立[J].食品科学,2012,33(19):249-253.
[9] 谢利芳,许志华,郭凯霞.2型糖尿病胰岛素抵抗研究进展[J].科学技术与工程,2010,10(15):3664-3669,3672.
[10] 安平,王安平,母义明.脂联素与胰岛素抵抗研究进展[J].生物技术通讯,2017,28(3):360-365.
[11] 郭燕,蔡艳,白云霞,等.血清脂联素、胰岛素抵抗与代谢综合征的相关性研究[J].中国实用医药,2016,11(29):8-10.
[12] 任毅,左之才,万涛梅.抵抗素在胰岛素抵抗中的作用机制及其受体信号通路研究进展[J].生理学报,2016,68(1):65-74.
[13] 王春炅,张园,管又飞,等.瘦素在糖脂代谢中的调控作用[J].中国生物化学与分子生物学报,2009,25(10):896-902.
[14] 周婧婧,高玉敏,赵灵燕.瘦素及瘦素受体与糖尿病关系的研究进展[J].内蒙古医学杂志,2016,48(4):442-444.
[15] 黄彩华,陈俊钦,林建新,等.运动改善2型糖尿病胰岛素抵抗与血清脂联素和瘦素及其交互作用[J].中国体育科技,2011,47(4):100-105.
[16] 马建,姚秀明,赵娜,等.祛胰抵方对2型糖尿病胰岛素抵抗大鼠PI-3K的影响[J].中医药学报,2013,41(5):50-53.
[17] 马建,马晓静,杜丽坤,等.祛胰抵方对2型糖尿病胰岛素抵抗大鼠骨骼肌细胞膜葡萄糖转运蛋白4的影响[J].医学研究杂志,2013,42(9):58-60.
[18] 闫玲玲,马建.祛胰抵方对2型糖尿病IR的临床观察[J].中医药学报,2012,40(1):113-115.