Effect of glucose-6-phosphate and pH on glucose transport in skeletal muscle plasma membrane giant vesicles

To study the interactions between insulin and contraction on the skeletal muscle glucose transport system, the hindquarters of male rats were perfused in the absence of insulin, in the presence of insulin (30 mU/ml), during contractions induced by sciatic nerve stimulation, or during contractions plus insulin. Compared with control preparations, rates of glucose uptake in the perfused hindquarter were increased by 2.5- and 2.6-fold in the insulin and insulin plus contraction groups, respectively, but not significantly increased in the contraction only preparations. After perfusion, soleus and red and white gastrocnemius muscles from the hindquarter were pooled and used for the preparation of plasma membranes. Skeletal muscle plasma membrane vesicle glucose transport rates were 2.2 +/- 0.5, 7.9 +/- 1.7, 9.0 +/- 2.2, and 10.8 +/- 2.0 nmol.mg protein-1.s-1 (40 mM glucose), and plasma membrane glucose transporter numbers were 4.7 +/- 0.5, 8.1 +/- 0.9, 9.1 +/- 1.0, and 8.6 +/- 0.6 pmol/mg protein in the control, contraction, insulin, and insulin plus contraction groups, respectively. The transport-transporter ratio, an indication of plasma membrane glucose transporter intrinsic activity, was increased by contraction, insulin, and insulin plus contraction. These results demonstrate that contractile activity in the absence of insulin increases muscle plasma membrane glucose transport by increasing transporter number and intrinsic activity. In addition, under these experimental conditions, the effects of insulin and contraction to increase muscle glucose transport are not additive.

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SKELETAL MUSCLE PLASMA MEMBRANE GLUCOSE TRANSPORT AND GLUCOSE TRANSPORTERS FOLLOWING EXERCISE.

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-198004001-00173 ◽

1980 ◽

Vol 21 (Supplement) ◽

pp. S29

Author(s):

L. J. Goodyear ◽

M. F. Hirshman ◽

P. A. King ◽

E. D. Horton ◽

E. S. Horton

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Glucose Transport ◽

Glucose Transporters ◽

Muscle Plasma Membrane

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Expression and cellular localization of glucose transporters (GLUT1, GLUT3, GLUT4) during differentiation of myogenic cells isolated from rat foetuses

Journal of Cell Science ◽

10.1242/jcs.107.3.487 ◽

1994 ◽

Vol 107 (3) ◽

pp. 487-496 ◽

Cited By ~ 3

Author(s):

I. Guillet-Deniau ◽

A. Leturque ◽

J. Girard

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Glucose Transport ◽

Cell Fusion ◽

Cellular Localization ◽

Glucose Transporter ◽

Glucose Transporters ◽

Short Exposure ◽

Myoblast Differentiation ◽

Igf I

Skeletal muscle regeneration is mediated by the proliferation of myoblasts from stem cells located beneath the basal lamina of myofibres, the muscle satellite cells. They are functionally indistinguishable from embryonic myoblasts. The myogenic process includes the fusion of myoblasts into multinucleated myotubes, the biosynthesis of proteins specific for skeletal muscle and proteins that regulates glucose metabolism, the glucose transporters. We find that three isoforms of glucose transporter are expressed during foetal myoblast differentiation: GLUT1, GLUT3 and GLUT4; their relative expression being dependent upon the stage of differentiation of the cells. GLUT1 mRNA and protein were abundant only in myoblasts from 19-day-old rat foetuses or from adult muscles. GLUT3 mRNA and protein, detectable in both cell types, increased markedly during cell fusion, but decreased in contracting myotubes. GLUT4 mRNA and protein were not expressed in myoblasts. They appeared only in spontaneously contracting myotubes cultured on an extracellular matrix. Insulin or IGF-I had no effect on the expression of the three glucose transporter isoforms, even in the absence of glucose. The rate of glucose transport, assessed using 2-[3H]deoxyglucose, was 2-fold higher in myotubes than in myoblasts. Glucose deprivation increased the basal rate of glucose transport by 2-fold in myoblasts, and 4-fold in myotubes. The cellular localization of the glucose transporters was directly examined by immunofluorescence staining. GLUT1 was located on the plasma membrane of myoblasts and myotubes. GLUT3 was located intracellularly in myoblasts and appeared also on the plasma membrane in myotubes. Insulin or IGF-I were unable to target GLUT3 to the plasma membrane. GLUT4, the insulin-regulatable glucose transporter isoform, appeared only in contracting myotubes in small intracellular vesicles. It was translocated to the plasma membrane after a short exposure to insulin, as it is in skeletal muscle in vivo. These results show that there is a switch in glucose transporter isoform expression during myogenic differentiation, dependent upon the energy required by the different stages of the process. GLUT3 seemed to play a role during cell fusion, and could be a marker for the muscle's ability to regenerate.

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Kinetics of glucose transport in rat skeletal muscle membrane vesicles: effects of insulin and contractions

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1992.262.5.e700 ◽

1992 ◽

Vol 262 (5) ◽

pp. E700-E711 ◽

Cited By ~ 11

Author(s):

T. Ploug ◽

H. Galbo ◽

T. Ohkuwa ◽

J. Tranum-Jensen ◽

J. Vinten

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Glucose Transport ◽

Cytochalasin B ◽

Equilibrium Distribution ◽

Initial Rate ◽

Membrane Vesicles ◽

Membrane Preparation ◽

Muscle Membrane ◽

Distribution Space

To study the mechanism of acceleration of glucose transport in skeletal muscle after stimulation with insulin and contractions, we isolated a subcellular vesicular membrane fraction, highly enriched in the plasma membrane enzyme K(+)-stimulated p-nitrophenylphosphatase and also enriched in some intracellular membranes. Protein recovery, morphology, lipid content, marker enzyme activities, total intravesicular volume, Western blot quantitation of GLUT-1, and glucose-inhibitable cytochalasin B binding were identical in membrane fractions from control, insulin-stimulated, contraction-stimulated, and insulin- and contraction-stimulated muscle. Time course of D-[3H]glucose entry in membrane vesicles at equilibrium exchange conditions showed that initial rate of transport at 30 mM of glucose was increased 19-fold and that equilibrium distribution space was increased 4-fold in vesicles from maximum stimulated muscle. The effects of insulin and contractions on initial rate of transport as well as on equilibrium distribution space were additive, and stimulation increased the substrate saturability of glucose transport. Furthermore, cytochalasin B binding to membranes prepared by using less centrifugation time than usual showed that, after stimulation with insulin and contractions, at least 35% of the total number of glucose transporters were redistributed from one kind of vesicles to a more slowly sedimenting kind of vesicles, probably reflecting translocation within the membrane preparation from intracellular vesicles to the plasma membrane upon stimulation. In the present membrane preparation the effects of insulin and/or contractions on glucose transport resemble those seen in intact muscle, and the effects are thus not dependent on cellular integrity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Stimulation of glucose transport in skeletal muscle by hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.4.1593 ◽

1991 ◽

Vol 70 (4) ◽

pp. 1593-1600 ◽

Cited By ~ 203

Author(s):

G. D. Cartee ◽

A. G. Douen ◽

T. Ramlal ◽

A. Klip ◽

J. O. Holloszy

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Muscle Contraction ◽

Glucose Transport ◽

Glucose Transporter ◽

Cytochalasin B ◽

Sugar Transport ◽

Transport Activity ◽

Hindlimb Muscles ◽

Stimulation Of

Hypoxia caused a progressive cytochalasin B-inhibitable increase in the rate of 3-O-methylglucose transport in rat epitrochlearis muscles to a level approximately six-fold above basal. Muscle ATP concentration was well maintained during hypoxia, and increased glucose transport activity was still present after 15 min of reoxygenation despite repletion of phosphocreatine. However, the increase in glucose transport activity completely reversed during a 180-min-long recovery in oxygenated medium. In perfused rat hindlimb muscles, hypoxia caused an increase in glucose transporters in the plasma membrane, suggesting that glucose transporter translocation plays a role in the stimulation of glucose transport by hypoxia. The maximal effects of hypoxia and insulin on glucose transport activity were additive, whereas the effects of exercise and hypoxia were not, providing evidence suggesting that hypoxia and exercise stimulate glucose transport by the same mechanism. Caffeine, at a concentration too low to cause muscle contraction or an increase in glucose transport by itself, markedly potentiated the effect of a submaximal hypoxic stimulus on sugar transport. Dantrolene significantly inhibited the hypoxia-induced increase in 3-O-methylglucose transport. These effects of caffeine and dantrolene suggest that Ca2+ plays a role in the stimulation of glucose transport by hypoxia.

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Insulin action on glucose transport and plasma membrane GLUT4 content in skeletal muscle from patients with NIDDM

Diabetologia ◽

10.1007/bf02658504 ◽

1996 ◽

Vol 39 (10) ◽

Cited By ~ 248

Author(s):

J. R. Zierath ◽

L. He ◽

A. Gumà ◽

E. Odegaard Wahlström ◽

A. Klip ◽

...

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Glucose Transport ◽

Insulin Action

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Glucose-induced insulin resistance of skeletal-muscle glucose transport and uptake

Biochemical Journal ◽

10.1042/bj2520733 ◽

1988 ◽

Vol 252 (3) ◽

pp. 733-737 ◽

Cited By ~ 55

Author(s):

E A Richter ◽

B F Hansen ◽

S A Hansen

Keyword(s):

Skeletal Muscle ◽

Glucose Uptake ◽

Glucose Transport ◽

Muscle Glycogen ◽

Insulin Action ◽

Insulin Stimulation ◽

Initial Values ◽

Muscle Glucose Transport ◽

Glycogen Stores ◽

Effect Of Glucose

The ability of glucose and insulin to modify insulin-stimulated glucose transport and uptake was investigated in perfused skeletal muscle. Here we report that perfusion of isolated rat hindlimbs for 5 h with 12 mM-glucose and 20,000 microunits of insulin/ml leads to marked, rapidly developing, impairment of insulin action on muscle glucose transport and uptake. Thus maximal insulin-stimulated glucose uptake at 12 mM-glucose decreased from 34.8 +/- 1.9 to 11.5 +/- 1.1 mumol/h per g (mean +/- S.E.M., n = 10) during 5 h perfusion. This decrease in glucose uptake was accompanied by a similar change in muscle glucose transport as measured by uptake of 3-O-[14C]-methylglucose. Simultaneously, muscle glycogen stores increased to 2-3.5 times initial values, depending on fibre type. Perfusion for 5 h in the presence of glucose but in the absence of insulin decreased subsequent insulin action on glucose uptake by 80% of the effect of glucose with insulin, but without an increase in muscle glycogen concentration. Perfusion for 5 h with insulin but without glucose, and with subsequent addition of glucose back to the perfusate, revealed glucose uptake and transport similar to initial values obtained in the presence of glucose and insulin. The data indicate that exposure to a moderately increased glucose concentration (12 mM) leads to rapidly developing resistance of skeletal-muscle glucose transport and uptake to maximal insulin stimulation. The effect of glucose is enhanced by simultaneous insulin exposure, whereas exposure for 5 h to insulin itself does not cause measurable resistance to maximal insulin stimulation.

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Isolation and properties of skeletal muscle plasma membrane

Biochimica et Biophysica Acta (BBA) - Biomembranes ◽

10.1016/0005-2736(73)90076-x ◽

1973 ◽

Vol 298 (3) ◽

pp. 593-607 ◽

Cited By ~ 86

Author(s):

Abdul M. Kidwai ◽

Martha A. Radcliffe ◽

Eda Y. Lee ◽

Edwin E. Daniel

Keyword(s):

Skeletal Muscle ◽

Plasma Membrane ◽

Muscle Plasma Membrane

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