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Disruption of microtubules in rat skeletal muscle does not inhibit insulin- or contraction-stimulated glucose transport
Ai, H; Ralston, E; Lauritzen, HPMM; Galbo, H; Ploug, T
关键词Cytoskeleton Metabolism Signaling Glucose Transporter 4 Exercise Colchicine Nocodazole
刊名AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
2003-10-01
DOI10.1152/ajpendo.00238.2002
285期:4页:E836-E844
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Endocrinology & Metabolism ; Physiology
研究领域[WOS]Endocrinology & Metabolism ; Physiology
关键词[WOS]3T3-L1 ADIPOCYTES ; GOLGI-COMPLEX ; TRANSFERRIN RECEPTOR ; GLUT4 DISTRIBUTION ; CYTOSKELETON ; TRANSLOCATION ; TRAFFICKING ; MYOGENESIS ; VESICLES ; FIBERS
英文摘要

Insulin and muscle contractions stimulate glucose transport in skeletal muscle through a translocation of intracellular GLUT4 glucose transporters to the cell surface. Judged by immunofluorescence microscopy, part of the GLUT4 storage sites is associated with the extensive microtubule cytoskeleton found in all muscle fibers. Here, we test whether microtubules are required mediators of the effect of insulin and contractions. In three different incubated rat muscles with distinct fiber type composition, depolymerization of microtubules with colchicine for less than or equal to 8 h did not inhibit insulin- or contraction-stimulated 2-deoxyglucose transport or force production. On the contrary, colchicine at least partially prevented the similar to30% decrease in insulin- stimulated transport that specifically developed during 8 h of incubation in soleus muscle but not in flexor digitorum brevis or epitrochlearis muscles. In contrast, nocodazole, another microtubule-disrupting drug, rapidly and dose dependently blocked insulin- and contraction-stimulated glucose transport. A similar discrepancy between colchicine and nocodazole was also found in their ability to block glucose transport in muscle giant "ghost" vesicles. This suggests that the ability of insulin and contractions to stimulate glucose transport in muscle does not require an intact microtubule network and that nocodazole inhibits glucose transport independently of its microtubule-disrupting effect.

语种英语
WOS记录号WOS:000185178200019
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被引频次:20[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56881
专题北京大学第三临床医学院_运动医学研究所
作者单位1.Univ Copenhagen, Panum Inst, Dept Med Physiol, Copenhagen Muscle Res Ctr, DK-2200 Copenhagen, Denmark
2.Bispebjerg Hosp, Dept Rheumatol, DK-2400 Copenhagen, Denmark
3.Peking Univ, Hosp 3, Inst Sports Med, Beijing 100083, Peoples R China
4.NIAMSD, Light Imaging Sect, NIH, Bethesda, MD 20892 USA
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Ai, H,Ralston, E,Lauritzen, HPMM,et al. Disruption of microtubules in rat skeletal muscle does not inhibit insulin- or contraction-stimulated glucose transport[J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,2003,285(4):E836-E844.
APA Ai, H,Ralston, E,Lauritzen, HPMM,Galbo, H,&Ploug, T.(2003).Disruption of microtubules in rat skeletal muscle does not inhibit insulin- or contraction-stimulated glucose transport.AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,285(4),E836-E844.
MLA Ai, H,et al."Disruption of microtubules in rat skeletal muscle does not inhibit insulin- or contraction-stimulated glucose transport".AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 285.4(2003):E836-E844.
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