[1]蔡琳婷,陈文新.心肌细胞葡萄糖转运蛋白4的转运调控及与心肌活力关系的研究进展[J].国际放射医学核医学杂志,2013,37(1):47-51.[doi:10.3760/cma.j.issn.1673-4114.2013.01.013]
 CAI Lin-ting,CHEN Wen-xin.Recent advances on the regulation of glucose transporter 4 transport and its relationship with myocardial viability in cardiomyocytes[J].International Journal of Radiation Medicine and Nuclear Medicine,2013,37(1):47-51.[doi:10.3760/cma.j.issn.1673-4114.2013.01.013]
点击复制

心肌细胞葡萄糖转运蛋白4的转运调控及与心肌活力关系的研究进展(/HTML)
分享到:

《国际放射医学核医学杂志》[ISSN:1673-4114/CN:12-1381/R]

卷:
37
期数:
2013年第1期
页码:
47-51
栏目:
综述
出版日期:
2013-01-25

文章信息/Info

Title:
Recent advances on the regulation of glucose transporter 4 transport and its relationship with myocardial viability in cardiomyocytes
作者:
蔡琳婷 陈文新
福建医科大学省立临床医学院核医学科, 福州, 350001
Author(s):
CAI Lin-ting CHEN Wen-xin
Department of Nuclear Medicine, Fujian Provincial Clinical College, Fujian Medical University, Fuzhou 350001, China
关键词:
葡萄糖转运蛋白质类易化性葡萄糖转运体4型肌细胞心脏心肌缺血
Keywords:
Glucose transport proteinsfacilitativeGlucose transporter type 4MyocytescardiacMyocardial ischemia
DOI:
10.3760/cma.j.issn.1673-4114.2013.01.013
摘要:
葡萄糖是心肌能量代谢的主要底物之一,在心肌缺血时是心肌的主要能量来源。葡萄糖通过细胞膜进入细胞内是心肌细胞葡萄糖代谢的第一步,也是心肌细胞利用葡萄糖的主要限速步骤。葡萄糖是依靠细胞膜上的葡萄糖转运蛋白(GLUTs)而进入细胞内的,GLUT4是心肌细胞主要的葡萄糖转运载体。GLUT4的质和量对心肌葡萄糖的跨膜转运起着决定性作用。因此,明确心肌葡萄糖转运及心肌细胞GLUT4的基因表达调控机制、转位调控机制、内在活性调控机制,对临床诊断心肌能量代谢性疾病具有重要意义。该文对近年来有关心肌葡萄糖转运及GLUT4调控方面的研究进行综述。
Abstract:
Glucose plays an important role in cardiac metabolism.It is the major energy source during myocardial ischemia.Trans-membrane glucose transport is the first rate-limited step for myocardial glucose metabolism,which is facilitated by glucose transports (GLUTs) and GLUT4 represents an important mechanism that governs the entry of glucose into the heart.The quality and quantity of GLUT4 play a decisive role in transmembrane glucose transport.To better retrieve myocardial metabolism and improve myocardial function under myocardial ischemia conditions,it is urgent to elucidate the regulatory mechanism of GLUT4 expression,the regulatory mechanism of GLUT4 translocation,the regulatory mechanism of GLUT4 intrinsic activity and glucose transport in cardiomyocytes.This review summarized the current state of knowledge regarding the regulation of GLUT4 functioning and glucose transport in cardiomyocytes.

参考文献/References:

[1] von Lewinski D,Gasser R,Rainer PP,et al.Functional effects of glucose transporters in human ventricular myocardium.Eur J Heart Fail,2010,12(2):106-113.
[2] Abel ED.Glucose transport in the heart.Front Biosci,2004,9:201-215.
[3] Steinbusch LK,Schwenk RW,Ouwens DM,et al.Subcellular traf-ficking of the substrate transporters GLUT4 and CD36 in car-diomyocytes.Cell Mol Life Sci,2011,68(15):2525-2538.
[4] Russell C,Stagg SM.New insights into the structural mechanisms of the COPII coat.Traffic,2010,11(3):303-310.
[5] Foley K,Boguslavsky S,Klip A.Endocytosis,recycling,and regu-lated exocytosis of glucose transporter 4.Biochemistry,2011,50(15):3048-3061.
[6] Schwenk RW,Dirkx E,Coumans W A,et al.Requirement for dis-tinct vesicle-associated membrane proteins in insulin-and AMP-activated protein kinase (AMPK)-induced translocation of GLUT4 and CD36 in cultured cardiomyocytes.Diabetologia,2010,53(10):2209-2219.
[7] Sheena A,Mohan SS,Haridas NP,et al.Elucidation of the glucose transport pathway in glucose transporter 4 via steered molecular dynamics simulations.PLoS One,2011,6(10):e25747.
[8] Stockli J,Fazakerley DJ,James DE.GLUT4 exocytosis.J Cell Sci,2011,124(24):4147-4159.
[9] Sparling DP,Griesel BA,Weems J,et al.GLUT4 Enhancer Factor(GEF) Interacts with MEF2A and HDAC5 to Regulate the GLUT4 Promoter in Adipocytes.J Biol Chem,2008,283(12):7429-7437.
[10] Magnoni LJ,Vraskou Y,Palstra AP,et al.AMP-activated protein kinase plays an important evolutionary conserved role in the regu-lation of glucose metabolism in fish skeletal muscle cells.PLoS One,2012,7(2):e31219.
[11] Holmes BF,Sparling DP,Olson AL,et al.Regulation of muscle GLUT4 enhancer factor and myocyte enhancer factor 2 by AMP-activated protein kinase.Am J Physiol Endocrinol Metab,2005,289(6):E1071-1076.
[12] Steinberg GH,Kemp BE.AMPK in Health and Disease.Physiol Rev,2009,89(3):1025-1078.
[13] Fujii N,Jessen N,Goodyear LJ.AMP-activated protein kinase and the regulation of glucose transport.Am J Physiol Endocrinol Metab,2006,291(5):E867-877.
[14] Li J,Miller EJ,Ninomiya-Tsuji J,et al.AMP-activated protein kinase activates p38 mitogen-activated protein kinase by increasing recruitment of p38 MAPK to TAB1 in the ischemic heart.Circ Res,2005,97(9):872-879.
[15] Montessuit C,Rosenblatt-Velin N,Papageorgiou I,et al.Regulation of glucose transporter expression in cardiac myocytes:p38 MAPK is a strong inducer of GLUT4.Cardiovasc Res,2004,64(1):94-104.
[16] Ojuka EO,Jones TE,Nolte LA,et al.Regulation of GLUT4 biogen-esis in muscle:evidence for involvement of AMPK and Ca2+.Am J Physiol Endocrinol Metab,2002,282(5):El008-1013.
[17] Huang S,Czech MP.The GLUT4 glucose transporter.Cell Metab,2007,5(4):237-252.
[18] Steinbusch LKM.CD36:a target to restore cardiac function in type 2 diabetes.Maastricht:Box press BV,Proefschriftmaken.nl,2011.
[19] Luiken JJ,Vertommen D,Coorl SL,et al.Identification of protein kinase D as a novel contraction-activated kinase linked to GLUT4-mediated glucose uptake,independent of AMPK.Cell Signal,2008,20(3):543-556.
[20] Egert S,Nguyen N,Schwaiger M.Contribution of alpha-adrenergic and beta-adrenergic stimulation to ischemia-induced glucose trans-porter (GLUT) 4 and GLUT1 translocation in the isolated perfused rat heart.Circ Res,1999,84(12):1407-1415.
[21] Wu-Wong JR,Berg CE,Dayton BD.Endothelin-stimulated glucose uptake:effects of intracellular Ca2+,cAMP and glucosamine.Clin Sci(Lond),2002,103 suppl48:S418-423.
[22] Stanley WC,Recchia FA,Lopaschuk GD.Myocardial substrate metabolism in the normal and failing heart.Physiol Rev,2005,85(3):1093-1129.
[23] d’Agostino C,Labinskyy V,Lionetti V,et al.Altered cardiac metabolic phenotype after prolonged inhibition of NO synthesis in chronically instrumented dogs.Am J Physiol Heart Circ Physiol,2006,290(4):H1721-1726.
[24] Depré C,Vanoverschelde JL,Goudemant JF,et al.Protection a-gainst ischemic injury by nonvasoactive concentrations of nitric ox-ide synthase inhibitors in the perfused rabbit heart.Circulation,1995,92(7):1911-1918.
[25] Sun D,Nguyen N,DeGrado TR,et al.Ischemia induces transloca-tion of the insulin-responsive glucose transporter GLUT4 to the plasma membrane of cardiac myocytes.Circulation,1994,89(2):793-798.
[26] Young LH,Renfu Y,Russell R,et al.Low-flow ischemia leads to translocation of canine heart GLUT-4 and GLUT-1 glucose trans-porters to the sarcolemma in vivo.Circulation,1997,95(2):415-422.
[27] Egert S,Nguyen N,Brosius FC 3rd,et al.Effects of wortmannin on insulin-and ischemia-induced stimulation of GLUT4 translocation and FDG uptake in perfused rat hearts.Cardiovasc Res,1997,35(2):283-293.
[28] McFalls EO,Murad B,Haspel HC,et al.Myocardial glucose uptake after dobutamine stress in chronic hibernating swine myocardium.J Nucl Cardiol,2003,10(4):385-394.
[29] Schertzer JD,Antonescu CN,Bilan PJ,et al.A transgenic mouse model to study glucose transporter 4myc regulation in skeletal muscle.Endocrinology,2009,150(4):1935-1940.
[30] Klocke R,Tian W,Kuhlmann MT,et al.Surgical animal models of heart failure related to coronary heart disease.Cardiovasc Res,2007,74(1):29-38.
[31] Zaha V,Nitschke R,Gobel H,et al.Discrepancy between GLUT4 translocation and glucose uptake after ischemia.Mol Cell Biochem,2005,278(1-2):129-137.
[32] Weiss RG,Chatham JC,Georgakopolous D,et al.An increase in the myocardial PCr/ATP ratio in GLUT4 null mice.FASEB J,2002,16(6):613-615.
[33] Belke DD,Larsen TS,Gibbs EM,et al.Glucose metabolism in per-fused mouse hearts overexpressing human GLUT-4 glucose trans-porter.Am J Physiol Endocrinol Metab,2001,280(3):E420-427.
[34] 龚菁,王红月,浦介麟,等.中华实验猪慢性心肌缺血心肌葡萄糖及脂肪酸代谢相关酶的变化.中华医学杂志,2008,88(31):2209-2213.
[35] Murray AJ,Lygate CA,Cole MA,et al.Insulin resistance,abnormal energy metabolism and increased ischemic damage in the chroni-cally infarcted rat heart.Cardiovasc Res,2006,71(1):149-157.
[36] McFalls EO,Murad B,Liow JS,et al.Glucose uptake and glycogen levels are increased in pig heart after repetitive ischemia.Am J Physiol Heart Circ Physiol,2002,282(1):H205-211.

备注/Memo

备注/Memo:
收稿日期:2012-08-23。
基金项目:福建省自然科学基金(项目编号:2010J01128)
通讯作者:陈文新,Email:wenxinchzt@yahoo.com.cn
更新日期/Last Update: 1900-01-01