GTF葛根功能牛奶的制备工艺及其对IGT小鼠的干预作用
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的:运用现代生物学技术,充分体现中医“治未病”的理论优势,利用奶牛的生物转化功能从富铬酵母中转化含高活性葡萄糖耐量因子(GTF)的功能牛奶,用中药活性成分葛根素组合制备而成GTF葛根功能牛奶,观察GTF葛根功能牛奶对葡萄糖耐量低减(IGT)小鼠的干预作用,通过对骨骼肌GLUT-4基因表达的影响来阐明其干预IGT的分子机制,为中西医结合方法干预治疗IGT提供新的思路。
     方法:(1)将奶牛随机分成四组,在奶牛饲料中分别添加不同剂量组的富铬酵母,通过检测牛奶中铬元素含量,观察牛奶铬含量与富铬酵母添加剂量的相关性。
     (2)采用D-半乳糖腹腔注射法诱导小鼠IGT模型,将GTF功能牛奶、普通牛奶、富铬酵母和二甲双胍分组灌胃,比较GTF功能牛奶与对照各组对IGT小鼠的干预作用。
     (3)从野葛中提取葛根素,与GTF功能牛奶按比例配制GTF葛根功能牛奶,初步完成GTF葛根功能牛奶的制备工艺。
     (4)采用D-半乳糖腹腔注射法诱导小鼠IGT模型,将GTF葛根功能牛奶按不同剂量分组灌胃,观察各组对IGT小鼠空腹血糖(FBG)、口服葡萄糖耐量试验(OGTT)、胰岛素耐量试验(ITT)、血清空腹胰岛素(FINS)和胰岛素抵抗指数(HOMA-IR)水平的影响。
     (5)采用逆转录-聚合酶链反应(RT-PCR)技术,通过检测经GTF葛根功能牛奶不同剂量组干预治疗后IGT小鼠骨骼肌组织葡萄糖转运蛋白4(GLUT-4)基因表达水平,来阐释GTF葛根功能牛奶对IGT小鼠干预作用的可能机制。
     结果:(1)牛奶铬含量与奶牛饲料中富铬酵母添加剂量两者高度相关。
     (2)GTF功能牛奶对IGT小鼠的干预作用与普通牛奶、富铬酵母组比较明显增强。
     (3)GTF葛根功能牛奶对IGT小鼠空腹血糖(FBG)无明显影响,降低口服葡萄糖耐量试验(OGTT)后2小时血糖(2hBG),增加胰岛素耐量试验(ITT)后胰岛素的敏感性,降低空腹胰岛素(FINS)和胰岛素抵抗指数(HOMA-IR)水平。
     (4)GTF葛根功能牛奶明显增加IGT小鼠骨骼肌组织葡萄糖转运蛋白4(GLUT-4)基因表达水平。
     结论:(1)饲料中添加的铬可经奶牛机体生物转化为高活性铬富集在牛奶中,牛奶中铬含量与饲料中铬含量呈正相关。
     (2)功能牛奶中的铬可能与牛奶中的多种氨基酸络合后形成葡萄糖耐量因子(GTF),调节葡萄糖代谢,对IGT小鼠起到干预作用。
     (3)葛根素与功能牛奶中的GTF组合后,药效上产生协同作用。
     (4)GTF葛根功能牛奶对IGT小鼠干预治疗的作用机制可能是通过增加外周靶细胞GLUT-4mRNA的表达,增强组织对葡萄糖的摄取,提高胰岛素敏感性从而干预治疗IGT的。
Objective: To study theory advantages in the Chinese medicine "Preventive Treatment of Disease" , using modern biological technology, utilize the biotransformation function of cows transforming the function of milk with high-activity glucose tolerance factor (GTF) form chromium-enriched yeast. Preparating GTF Puerarin function milk form Chinese medicine active ingredients Puerarin, to observe the role of intervention to the function of GTF Puerarin milk on Grape impaired glucose tolerance (IGT) in mice, through skeletal muscle GLUT-4 gene expression to clarify its molecular mechanism of intervention on IGT, to provide new ideas for traditional Chinese and western medicine in the treatment of IGT intervention.
     Methods: (1) Dividing randomly the cows into four groups, to add the chromium-rich yeast to dairy cattle feed at different dose groups respectively, through the detection of chromium content in milk to conclude the relationship between milk chromium content and chromium-rich yeast additive dosage.
     (2)Choosing GTF functions milk, ordinary milk, chromium-rich yeast and metformin to lavage stomatch to impaired glucose tolerance (IGT) mice model induced by D-galactose peritoneum injection, to compare the intervention role on the IGT mice between the milk GTF functions and each control group.
     (3) Extracting Pueraria lobata Puerarin form wilding Puerarin with GTF function of milk in proportion to the preparation of GTF functions Puerarin milk, to achieve initially GTF Puerarin functional milk production process.
     (4)Adopting D-galactose in mice induced by intraperitoneal injection of IGT model, GTF Puerarin milk will function by gavage administration in different doses, to observe each group of mice IGT fasting blood glucose (FBG),oral glucose tolerance test (OGTT), insulin tolerance test (ITT),serum fasting insulin (FINS) and insulin resistance index (HOMA-IR) levels.
     (5)Applying Reverse transcriptase-polymerase chain reaction (RT-PCR) technology,though detecting Puerarin by GTF function of different doses of milk after treatment IGT intervention group of mice skeletal muscle glucose transporter 4 (GLUT-4) gene expression level, to explain the possible mechanism of GTF Puerarin functional milk interfere role in IGT mice.
     Results: (l)There were significant correlations between Chromium content of milk and volume of dairy feed additive chromium-rich yeast.
     (2) Compared with ordinary milk group, chromium-rich yeast group, GTF functions milk intervention on the role of IGT in mice increased.
     (3)GTF Puerarin functional milk of mice IGT fasting blood glucose (FBG) had no significant effect, reduced oral glucose tolerance test (OGTT) 2 hours after glucose (2hBG), increased insulin tolerance test (ITT) after the insulin sensitivity, lowered fasting insulin (FINS) and insulin resistance index (HOMA-IR) levels.
     (4)GTF Puerarin functional milk IGT mice significantly increased skeletal muscle glucose transporter 4 (GLUT-4) gene expression level.
     Conclusion: (1)Chromium diet dairy organism biology may be translated into highly active chromium enrichment in the milk, the milk in the chromium content and chromium content of feed was positively correlated.
     (2) Function of milk in the milk may be associated with chromium in a variety of amino acids formed after complexation glucose tolerance factor (GTF), regulation of glucose metabolism on the IGT intervention played a role in mice.
     (3) After Puerarin and function of milk composed with GTF assembling, the efficacy had a synergistic effect.
     (4)The role of mechanisms GTF Puerarin functional milk intervention on the treatment of IGT in mice was possible increasing the peripheral target cells the expression of GLUT-4mRNA to enhance the uptake of glucose Organize, improved insulin sensitivity.
引文
[1]卢艳慧,陆菊明.糖耐量低减的流行病学及危害[J].实用糖尿病杂志,2007,3(6):3-4.
    [2]Alexander M K.Improving enzymes by using them in organic solvents[J].Nature,2001,409(11):241-246.
    [3]王志耕,陈文静,韩雪峰,等.富锗牛奶的研究[J].安徽农业大学学报,2002,29(3):279-282.
    [4]Schwarz K,Mertz W.Chromium(Ⅲ)and glucose tolerance factor[J].Arch Biochem Biophys,1959,85(1):292.
    [5]刘大星,闫祥华,王修德.人体微量元素铬与糖尿病的关系[J].实用医药杂志,2005,22(6):556-558.
    [6]Yamamoto A.Purifcation and properties of biologically active chromium complex from bovine colostrums[J].J Nutr,1988,18:39.
    [7]洪敏,李新生,颜雪明,等.含铬有机化合物的生物活性及研究进展[J].化工时刊,2004,18(1):9-12.
    [8]王少康.亚急性衰老动物模型的建立及评价[J].东南大学学报·医学版,2002,21(3):217-220.
    [9]方朝晖,崔宜武,陈晓雯,等.茶色素对大鼠D-半乳糖性白内障的影响[J].安徽中医学院学报,1997,16(3):53-55.
    [10]潘竞锵,李博萍,谭海荣,等.中药对D-半乳糖诱导病理模型作用的研究进展[J].广东药学2001,11(5):1-5.
    [11]林佳,潘竞锵,李博薄,等.黄连D-半乳糖诱导大鼠血糖和糖耐量减退影响的实验研究[J].中国临床医药研究杂志,2005,139:15045-15047.
    [12]Lin HZ,Yang SQ,Chukaree C,et al.Meformin reverses fatty liver disease in obese,leptin deficient mice[J].Nat Med,2000,6:998.
    [13]张瞳,许峰,周波,等.富铬酵母的应用与展望[J].生物技术通报,2006年增刊:106-108.
    [14]柏芳表,金仲品.铬与人体健康和疾病[J].微量元素与健康研 究,2002,19(4):77-78.
    [15]孔令芳,张静,钱聪,等.铬与2型糖尿病[J].中国医院药学杂志,2006,26(5):606-607.
    [16]卢艳花.中药有效成分提取分离实例[M].北京:化学工业出版社,2007,1:80.
    [17]杨东晖,陈浪,曾志,等.葛根化学成分的研究[J].华南师范大学学报(自然科学版),2002,4:94-97.
    [18]梅林,石开云,杨元娟,等.葛根中葛根素的分离纯化技术进展[J].广州化学,2007,32(1):73-76.
    [19]于丽萍.系列牛奶保健品[J].四川奶业,2003,4:19-20.
    [20]刘吉昌,柴春雨.提升中国乳业国际竞争力问题研究[J].世界农业,2006,6:23-26.
    [21]林维宣,薛维政.国内外食品标准大全[M].大连:大连海事大学出版社,1997:580-582.
    [22]康怀彬.无公害牛奶加工技术[J].河南农业科学,2003,8:68-69.
    [23]王标,周伦江,庄向生.畜产品卫生安全同题及对策[J].福建畜牧兽医,2002,24(5):36.
    [24]袁建敏,马红兵.畜产品安全与标准化[J].中国农业科技导报,2002,4(5):31.
    [25]赵铁耘,李秀钧.糖尿病诊治研究新理念[J].中国实用内科杂志,2005,25(4):302-304.
    [26]张海燕,刘国良.IGT干预研究简介与评议[J].辽宁实用糖尿病杂志,2004,12(6):5-6.
    [27]杨文英.2型糖尿病的治疗从1GT起步的新认识与评价[J].实用糖尿病杂志,2000,8(4):12.
    [28]康格非.临床生物化学和生物化学检验[M].第2版.北京:人民卫生出版社,1998,36-45.
    [29]周丽斌,杨颖,尚文斌,等.小檗碱改善高脂饮食大鼠的胰岛素抵抗[J]. 放射免疫学杂志,2005,18(3):198-200.
    [30]热阳古丽·沙塔尔,古力扎·库尔班.罗格列酮在IGT期六个月的临床观察[J].中华临床医学研究杂志,2007,13(18):2631-2632.
    [31]刘超.TRIPOD研究简介与评议[J].辽宁实用糖尿病杂志,2004,12(6):7-9.
    [32]Bonora E,Targher G,Alberiche M,et al.Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity[J].Diabetes Care,2000,23:57-63.
    [33]时培玲,付传花,姚国民.葛根在非解表作用中的应用[J].河南中医药学刊,1999,14(1):50.
    [34]于健,苏珂.葛根素对2型糖尿病病人胰岛素抵抗的影响[J].中国新药与临床杂志,2002,21(10):58-57.
    [35]韩会民,王树国.葛根素治疗非胰岛素依赖型糖尿病患者胰岛素抵抗的研究[J].中国中西医结合急救杂志,2006,3(13):117-119.
    [36]Bradbury J.Added chrominum may help type 2diabetics[J].Lancet,1997,350:1453.
    [37]Defrono R A.The triumvirate:β-cell,muscle,liver A collusion responsible for NIDDM[J].Diabetes,1988,37(6):667-687.
    [38]Zisman A,Peroni O D,Abel E D.Targeted disruption of the glucose transporter 4 selectively in muscle cause insulin resistance and glucose intolerance[J].Nature Med,2000,6(8):924-928.
    [39]Karlsson M,Thorn H,Parpal S,et al.Insulin induces translocation of glucose transporter GLUT4 to plasma membrane caveolae in adipocytes[J].FASEBJ,2002,16:249.
    [40]Furtado LM,Somwar R,Sweeney G,et al.Activation of the glucose transporter GLUT4 by insulin[J].Biochem Cell Biol,2002,80:569-578
    [41]张敬芳,王光浩.黄芪多糖对2型糖尿病大鼠骨骼肌组织GLUT4表达的影响[J].时珍国医国药,2007,18(11):2652-2653.
    [42]Le Roith D,Zick Y.Recent advances in our understanding of insulin action and insulin resistance[J].Diabetes Care,2001,24(3):588-597.
    [43]Shintani M,NishimuranH,Yonemitsu S,et al.Troglitazone not only increases GLUT4 but also induces its translocation in rat adipolytes[J].Diabetes,2001,50(10):2296-2300.
    [44]杨文英.2型糖尿病的防治势必超前并落实到糖耐量减低阶段[J].辽宁实用糖尿病杂志,2004.12(2):3-5.
    [45]杨霞,白永清.中西医对糖耐量异常的认识及研究现状[J].山西中医,2008,24(3):53-55.
    [46]卢艳慧,陆菊明.糖耐量减低必须治疗[J].临床内科杂志,2006,23(2):141-142.
    [47]杨文英,林丽香,齐今容,等.阿卡波糖和二甲双胍对IGT人群糖尿病预防的效果[J].中华内分泌代谢杂志,2001,17(3):131-134.
    [48]吕仁和,肖永华,刘滔波.分期论治糖尿病[J].药品评价,2008,5(1):35-37.
    [49]仝小林.让中医药走向世界.人民日报,2004-11-4(15).
    [50]潘秋,周丽波,仝小林.从糖尿病前期谈“治未病”[J].中华中医药杂志,2008,23(3):191-193.
    [51]陈霞波.糖耐量低减与脾不散精[J].浙江中医杂志,2005,40(3):118-119.
    [52]冯凭.葡萄糖耐量低减[J].国外医学内分泌学分册,2002,22(6):345-346.
    [53]王先令.糖耐量低减的干预治疗[J].前卫医药杂志,2001,18(5):385-386.
    [54]余峰彬.胰岛素抵抗的分子机制[J].攀枝花学院学报,2004,21(6):117-120.
    [55]陈家伦.餐后高血糖(IGT)的重要性及防治[J].中华内分泌代谢杂 志.1998,14(5):327-330.
    [56]Larsson H,Ahren B.Relative hyperproinsulinemia as a sign of islet dysfunction in women with impaired glucose tolerance.J Clin Endocrinol Metab,1999,84(6):2068-2074.
    [57]王先令,陆菊明.糖耐量低减的病理生理[J].天津医药,2002,30(3):187-189.
    [58]DeFronzo RA,Tobin JD,Andres R.Glucose clamp technique:a method for quantifying insulin secretion and resistance[J].Am J Physiol,1979,237(3):E214-223.
    [59]Wasada T,Kuroki H,Katsumori K,et al.Who are more insulin resistant,people with IFG or people with IGT[J]?Diabetologia,2004,47(4):758-759.
    [60]Festa A.D' Agostino R Jr,Hanley AJ.et al.Differences in insulin resistance in nondiabetic subjects with isolated impaired glucose tolerance or isolated impaired fasting glucose[J].Diabetes,2004,53(6):1549-1555.
    [61]Van Haeften TW,Piments W,Mitrskou A,et al.Disturbances in β-cell function in impaired fasting glycemis[J].Diabetes,2002,51(Suppl.1):S265-S270.
    [62]Pimenta WP,Santos mL,Cruz NS,et al.Brazilian individuals with impaired glucose tolerance are characterized by impaired insulin secretion[J].Diabetes metab,2002,28(12):468-476.
    [63]郑信华,池莲祥,刘香萍,等.糖调节受损的胰岛素抵抗与胰岛β细胞功能研究新进展[J].海南医学,2008,19(3):138-141.
    [64]翁工清.葛根健脾益肾通脉醒脑的补益作用[J].中草药,2000,31(6):附2-3.
    [65]翁工清.葛根补益功用纵览[J].山东中医杂志,2001,20(5):363.
    [66]罗助荣,盖晓波,郏卫星,等.葛根素治疗不稳定型心绞痛及对凝血纤溶 活性和内皮功能的影响[J].中国中西医结合急救杂志,2000,7:105-106.
    [67]周运鹏.葛根素药理作用和临床应用研究进展[J].中西医结合杂志,1984,4:699.
    [68]李妮.葛根素对糖尿病患者糖化血红蛋白丙二醛及超氧化物歧化酶的影响[J].广西医学,1997,19:963.
    [69]朱西庚.微量元素铬与糖尿病[J].糖尿病之友,2005,8:61.
    [70]Cefalu WT,Hu FB.Role of chromium in human health and in diabetes[J].Diabetes Care.2004.27(11):2741.
    [71]柏芳表,金仲品.铬与人体健康和疾病[J].微量元素与健康研究,2002,19(4):77-78.
    [1]郭仪,石岩.葡萄糖转运蛋白4转位与胰岛素抵抗[J].辽宁中医药大学学报,2007,9(4):63-64.
    [2]Haffner S M,Kennedy E,Gonzalez C,et al.A prospective analysis of the HOMA model:the mexico city diabetes study[J].Diabetes Care,1996,19:1138-1141.
    [3]Joost H,Thorens B.The extended GLUT-family of sugar/polyol transport facilitators:Nomenclature,sequence,characteristic and potential function of its novel members[J].Molecular Membrane Biol,2001,18:247-256.
    [4]Bryant N,Govers R,James D,et al.Regulated Transport Of The Glucose Transporter GLUT4[J].Nat Rev Mol Cell Biol,2002,3(4):267-277.
    [5]Watson R,Pessin J.Intracellular organization of insulin signaling and GLUT4 translocation[J].Recent Prog Horm Res,2001,56:175-193.
    [6]Bell G,Polonsky K.Diabetes mellitus and genetically programmed defects in β-cell function[J].Nature.2001.414:788-791.
    [7]Mueckler M,Caruso C,Baldwin SA,et al.Sequence and structure of a human glucose transporter[J].Science.1985,229:941.
    [8]邱凯,高宏凯,蔡晓军.葡萄糖转运蛋白4与骨骼肌、脂肪组织胰岛素抵抗的关系[J].中国实用医药,2008,3(3):129-130.
    [9]Zorzano A,Munoz P,Camps M,et al.Insulin-induced redistribution of GLUT4 glucose carriers in the muscle fiber[J].Diabetes,1996,45:70.
    [10]Marette A,Richardson JM,Ramlal T,et al.Abundance,localization,and insulin 2 induced translocation of glucose transporters in red and white muscle[J].Am J Phsiol,1992,263:C4432452.
    [11]Jaquet D,Vidal H,HankardR,et al.Impaired regulation of glumes transporter 4 gene expression in insulin resistance associated with in utero undernutrition[J].J Clin Endocrinol Metab,2001,86(7):3266-3271.
    [12]Maianu L,Keller SR,Garvey WT.Adipocytes exhibit abnormal subcellular distribution and transloration of veieles containing glucose transporter 4 and insulin-regulated amino peptidase in type2 diabetes mellitus:implications tegartling defects in vesicle tracking.J Clin Endocrinol Melab,2001,86(11):5450-5456.
    [13]Bruzinick JT.GLUT4 over expression in db/db mice,lose dependently ameliorates diabetes but is not a life long cure[J].Diabetes,2001,50(3):593-600.
    [14]Abel ED,Peroni O,Kim JK,et al.Adipose selective targeting of the GLLT4 gene impairs insulin action in muscle and liver[J].Nature,2001,409(6821):729-733.
    [15]Tozzo E,Gnudi L,Kahn BB.Amelioration of insulin resistance in steroptozotoc in diabetes mice by transgenic over expression of GLUT4 driver by an adipose specific promoter[J].Endocrinology, 1997,138(4):1604-1611.
    [16]高磊,刘绛光.对葡萄糖转运蛋白的讨论[J].国外医学临床生化与检验学分册,1999,20(6):131.
    [17]李新荣,章立,徐蘅.2型糖尿病与胰岛素信号领导缺陷关系的研究[J].中国糖尿病杂志,2000,8(5):266.
    [18]Michael Gaster,Peter Staehr,Henning Beck-Nielsen,et al.GLUT4is reduced in slow muscle fibers of type 2 diabetic patients[J].Diabetes,2001,50(6):1324.
    [19]Seung Y,Park,WanLee.The depletion of cellular mitochondrial DNA causes insulin resistance through the alteration of insulin receptor substrate-1 in rat myocytes[J].Diabetes Research and Clinical Practice,2007,1:51.
    [20]毕会民,欧阳静萍,邓向群,等.胰岛素抵抗大鼠骨骼肌中蛋白激酶B 表达及葡萄糖转运蛋白4转位的改变[J].中华糖尿病杂志,2005,8:13-14
    [21]Nelson B A,Robinson K A,Buse M G.High glucose and glucosamine induce insulin resistance via different mechanisms in 313-L1adiposities[J].Diabetes,2000,49:981-991.
    [22]Zierath J R,Krook A,Wallberg-Renriksson H.Insulin action in skeletal muscle from patients with NIDDM[J].Mol Cell Biochem,1998,182:153-160.
    [23]Maier V H,Gould G W.Long-term insulin treatment of 3T3-E1adipocytes results in mis-targeting of GLUT4:implications for insulin-stimulated glucose transport[J].Diabetologia,2000,43:1273-1281.
    [24]Xing A Y,Challier J C,Lepercq J,et al.Unexpected expression of glucose transporter 4 in villous stromal ceils of human placenta[J].Clin Endocrinol Metab,1998,83:4097-4101.
    [25]James D J,Caims F,Salt I P,et al.Skeletal muscle of stroke-prone spontaneously hypertensive rats exhibits reduced insulin-stimulated glucose transport and elevated levels of cave olio and flotillin [J].Diabetes,2001,50:2148-2156.
    [26]de Carvalho Papa P,Vargas A M,da Silva J L, et al. GLUT4 protein is differently modulated during development of obesity in monosodium glutamate-treated mice[J]. Life Sci, 2002, 71(16): 1917.
    [27]Schwartznberg-Bar-Yoseph F, Armoni M,Karnieli E. The tumor suppressor p53 down-regulates glucose transporters GLUTl and GLUT4 gene expression [J]. Cancer Res, 2004, 64(7): 2627.
    [28]Yoshikawa T,Noguchi Y,Satoh S.Inhibition of IRS-1 phosphorylation and the alterations of GLUT4 in isolated adipocytes from cachectic tumor-bearing rats[J]. Biochem Biophys Res Commun. 1999,256:676-681.
    [29]Noguchi Y,Yoshikawa T,Marat D, et al. Insulin resistance in cancer patients is associated with enhanced TNF-alpha expression in skeletal muscle[J]. Biochem Biophys Res Commun, 1998, 253: 887-892
    [30] Jaquet D, Gaboriau A, Czemichow P, et al. Insulin resistance early in adulthood in subjects bern with intrauterine growth retardation[J].Clin Endocrinol Metab, 2000, 85: 1401-1406.
    [31] Jaquet D, Vidal H, Hankard R, et al. Impaired regulation of glucose transporter 4 gene in insulin resistance associated with in uteroundernutrition [J].Clin Endocrinol Metab, 2001, 86: 3266-3271.
    [32] Takabashi Y, Ide T. Dietary n-3 fatty acids affect mRNA level of brown adipose tissue uncoupl ing protein 1, and white adipose tissue leptin and glucose transporter 4 in the rat[J].Br J Nutr, 2000,84: 175-184.
    [33]Kristiansen S,Gade J,Wojtaszewski J F, et al.Glucose uptake is increased in trained vs.untrained muscle during heavy exercise[J].Appl physiol,2001,89:1151-1158.
    [34]Charron MJ,Katz EB,Olson AL.GLUT4 Gene Regulation and Manipulation[J].J Biol Chem.1999.274(6):3253-3256.
    [35]Dela F,Ploug T,Handberg A,et al.Physical training increases muscle GLUT4 protein and mRNA in patients with NIDDM[J].Diabetes.1994.43(7):862-865.
    [36]Detaille D,Wiernsperger N,Devos P.Metformin interaction with insulin-regulated glucose uptake,using the Xenopus laevis oocyte model expressing the mammalian GLUT4[J].Eur J Pharmacol,1999,377:127-136.
    [37]Le Roith D,Zick Y.Recent advances in our understanding of insulin action and insulin resistance[J].Diabetes Care,2001,24(3):588-597.
    [38]文重远,吴勇,李燕,等.2型糖尿病大鼠心肌葡萄糖转运体4的变化及其对葡萄糖和脂肪酸代谢的影响[J].中华医学杂志,2005,85(21):1460-1463.
    [39]Stephens JM,Lee J,Pilch FP.Tumor necrosis factor α induced insulin resistance in 3T3-C adipocyte is accompanied by a loss of insulin receptor sabstrate21 and GLUT4 expression without a loss of insulin receptor mediated signal transduction[J].J Biol Chem,1997,272(2):971-976.
    [40]Tsao TS,Stenbit AE,Factor SM,et al.Prevention of insulin resistance and diabetes in mice heterozygous for GLUT4 ablation by transgenic complementation of GLUT4 in skeletal muscle[J].Diabetes,1999,48:775-782.
    [41]Brozinick JT Jr,Mc Coid SC,Reynolds TH,et al.GLUT4 over expression in db/db mice dose-dependently ameliorates diabetes but is not a lifelong cure[J].Diabetes,2001,50:593-600.
    [42]王东.胰岛素抵抗的中医药治疗进展[J].江西中医药,2006,37(282):60-62.
    [43]柴可夫,覃志成,王亚丽.北五味子油对糖尿病小鼠抗氧化及葡萄糖转运蛋白4mRNA表达的影响[J].中医药学刊,2006,24(7):1199-1201.
    [44]李娟娟,毕会民.葛根素对胰岛素抵抗大鼠脂肪细胞葡萄糖转运蛋白4的影响[J].中国临床药理学与治疗学,2004,9(8):885-888.
    [45]毛先晴,欧阳静萍,吴勇,中药黄芪多糖对糖尿病大鼠心肌GLUT4表达的影响[J].武汉大学学报(医学版),2005,26(4):457-459.
    [46]邝秀英,朱章志,邓常青,等.益气活血通腑法对类2型糖尿病大鼠骨髂肌GLUT4表达的影响[J].中国中医基础医学杂志,2003,9(10):34-38.
    [47]陈广,陆付耳,徐丽君.黄连解毒汤对2型糖尿病大鼠靶组织葡萄糖转运子4的影响[J].中西医结合学报,2007,5(4):412-415.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700