Role for the microtubule cytoskeleton in GLUT4 vesicle trafficking and in the regulation of insulin-stimulated glucose uptake

FLETCHER, L. M.; WELSH, G. I.; OATEY, P. B; TAVARÉ, J. M.

doi:10.1042/0264-6021:3530735u

Cited by 31 publications

(44 citation statements)

References 25 publications

(52 reference statements)

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“…A number of studies had shown that both microtubules and actin filaments participated in insulin-induced glucose uptake. Previous works on microtubule depolymerization (Chen et al, 2008;Fletcher et al, 2000;Olson et al, 2001) or kinesin perturbation (Emoto et al, 2001;Semiz et al, 2003) supported the notion that microtubule is obligatory to insulin-stimulated GLUT4 translocation and glucose uptake, but results were not consistent (Molero et al, 2001;Shigematsu et al, 2002). Formation of cortical actin, as manifested by membrane ruffles had been reported following insulin stimulation in muscle and fat cells (Khayat et al, 2000;Tong et al, 2001).…”

Section: Introductionmentioning

confidence: 66%

Microtubule network is required for insulin-induced signal transduction and actin remodeling

Liu

Cheung

Lan

et al. 2013

Molecular and Cellular Endocrinology

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Section: Introductionmentioning

confidence: 66%

Microtubule network is required for insulin-induced signal transduction and actin remodeling

Liu

Cheung

Lan

et al. 2013

Molecular and Cellular Endocrinology

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“…Despite that, clonal cell lines are genetically stable; the phenotype of the differentiated myotube depends heavily on the protocol used to induce differentiation (45). Alternatively, other studies probing GLUT4 traffic necessitated the use of mononuclear systems such as L6 myoblasts or non-muscle cell types such as 3T3-L1 fibroblasts and 3T3-L1 adipocytes (14,17,47). These cell models are imperative in assessing various aspects of GLUT4 cell biology but are further removed from mature skeletal muscle.…”

Section: Cell Systems Used To Study Glut4 Translocation With High Spamentioning

confidence: 98%

Measuring GLUT4 translocation in mature muscle fibers

Lauritzen

Schertzer

2010

American Journal of Physiology-Endocrinology and Metabolism

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Skeletal muscle is the major tissue for postprandial glucose disposal. Facilitated glucose uptake into muscle fibers is mediated by increases in surface membrane levels of the glucose transporter GLUT4 via insulin- and/or muscle contraction-mediated GLUT4 translocation. However, the regulatory mechanisms controlling GLUT4 translocation in skeletal muscle have been difficult to characterize at the cell biology level due to muscle tissue complexity. Muscle cell culture models have improved our understanding of GLUT4 translocation and glucose transport regulation, but in vitro muscle models lack many of the characteristics of mature muscle fibers. Thus, the molecular and cellular details of GLUT4 translocation in mature skeletal muscle are deficient. The objective of this review is to highlight how advances in recent experimental approaches translate into an enhanced understanding of the regulation of GLUT4 translocation and glucose transport in mature skeletal muscle.

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“…Depolymerisation of microtubules does not affect insulin-stimulated glucos e transport in cultures of L6 muscle cells (Tsakiridis et al 1994) or insulin-and contraction-stimulated glucose transport in incubated rat muscles (Ai et al, unpublishe d data). In 3T3-L1 cultured adipocytes , in contrast, a sizeable decreas e in insulin-induced GLUT4 translocation (40± 80%) has been reported (Fletcher et al 2000, Guilherm e et al 2000, Emoto et al 2001, Olson et al 2001. New results , however, sugges t that the effect obs erved in 3T3-L1 adipocytes is not due to microtubule disruption but to a direct inhibition of GLUT4 transport activity by nocodazole, the drug us ed to disrupt microtubules (Molero et al 2001).…”

Section: Is the Cytoskeleton Involved In Glut4 Localization And Transmentioning

confidence: 78%

Exploring the whereabouts of GLUT4 in skeletal muscle (Review)

Ploug¹,

Ralston²

2002

Molecular Membrane Biology

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The glucose transporter GLUT4 is expressed in muscle, fat cells, brain and kidney. In contrast to other glucose transporters, GLUT4 in unstimulated cells is mostly intracellular. Stimuli such as insulin and muscle contractions then cause the translocation of GLUT4 to the cell surface. Questions related to GLUT4 storage compartments, trafficking to the surface membrane, and nature of the intracellular pools, have kept many groups busy for the past 20 years. Yet, one of the main questions in the field remains the universality of GLUT4 features. Can one extrapolate work done on fat cells to muscle or brain? Or vice-versa? Can one use cultures to predict GLUT4 behaviour in fully differentiated tissues? This review summarizes the authors' knowledge of GLUT4 biology in skeletal muscle, which is the predominant tissue for glucose homeostasis. The results are compared to those obtained with the fat cell system, and an attempt is made to assess the universality principle.

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Role for the microtubule cytoskeleton in GLUT4 vesicle trafficking and in the regulation of insulin-stimulated glucose uptake

Cited by 31 publications

References 25 publications

Microtubule network is required for insulin-induced signal transduction and actin remodeling

Microtubule network is required for insulin-induced signal transduction and actin remodeling

Measuring GLUT4 translocation in mature muscle fibers

Exploring the whereabouts of GLUT4 in skeletal muscle (Review)

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