Low-Flow Ischemia Leads to Translocation of Canine Heart GLUT-4 and GLUT-1 Glucose Transporters to the Sarcolemma In Vivo

Circulation ◽  
1997 ◽  
Vol 95 (2) ◽  
pp. 415-422 ◽  
Author(s):  
Lawrence H. Young ◽  
Yin Renfu ◽  
Raymond Russell ◽  
Xiaoyue Hu ◽  
Michael Caplan ◽  
...  
Keyword(s):  
Glucose Transporters ◽  
Low Flow ◽  
Canine Heart ◽  
Glut 1 ◽  
Glut 4

Effect of in vivo injection of cholera and pertussis toxin on glucose transport in rat skeletal muscle

1997 ◽  
Vol 272 (1) ◽  
pp. E7-E17 ◽  
Author(s):  
T. Ploug ◽  
X. Han ◽  
L. N. Petersen ◽  
H. Galbo
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Pertussis Toxin ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Glut 1 ◽  
Glut 4 ◽  
Gastrocnemius Muscles ◽  
Muscle Glucose Transport

Cholera toxin (CTX) and pertussis toxin (PTX) were examined for their ability to inhibit glucose transport in perfused skeletal muscle. Twenty-five hours after an intravenous injection of CTX, basal transport was decreased approximately 30%, and insulin- and contraction-stimulated transport was reduced at least 86 and 49%, respectively, in both the soleus and red and white gastrocnemius muscles. In contrast, PTX treatment was much less efficient. Impairment of glucose transport appeared to develop 10-15 h after CTX administration, which coincided with development of hyperglycemia despite hyperinsulinimia, increased plasma free fatty acid levels, increased adenosine 3',5'-cyclic monophosphate (cAMP) concentrations in muscle, but no difference in plasma catecholamines. Twenty-five hours after CTX treatment, GLUT-4 protein in both soleus and red gastrocnemius muscles was decreased, whereas no change in GLUT-1 protein content was found. In contrast, GLUT-4 mRNA was unchanged, but transcripts for GLUT-1 were increased > or = 150% in all three muscles from CTX-treated rats. The findings suggest that CTX via increased cAMP impairs basal as well as insulin- and contraction-stimulated muscle glucose transport, at least in part from a decrease in intramuscular GLUT-4 protein.

Protection of ischemic hearts by high glucose is mediated, in part, by GLUT-4

2001 ◽  
Vol 281 (1) ◽  
pp. H290-H297 ◽  
Author(s):  
Ravichandran Ramasamy ◽  
Yuying C. Hwang ◽  
John Whang ◽  
Steven R. Bergmann
Keyword(s):  
High Glucose ◽  
Cytochalasin B ◽  
Glucose Transporters ◽  
Left Ventricular ◽  
Ischemic Myocardium ◽  
Low Flow ◽  
Glut 4 ◽  
Rat Hearts ◽  
Percent Recovery ◽  
Normal Glucose

Metabolic interventions that promote glucose use during ischemia have been shown to protect ischemic myocardium and improve functional recovery on reperfusion. We evaluated whether the cardioprotection afforded by high glucose during low-flow ischemia is associated with changes in the sarcolemmal content of glucose transporters, specifically GLUT-4. Isolated rat hearts were paced at 300 beats/min and perfused under normal glucose (5 mM) or high glucose (10 mM) conditions in buffer containing 0.4 mM albumin, 0.4 mM palmitate, and 70 mU/l insulin and subjected to 50 min of low-flow ischemia and 60 min of reperfusion. To determine the importance of insulin-sensitive glucose transporters in mediating cardioprotection, a separate group of hearts were perfused in the presence of cytochalasin B (10 μM), a preferential inhibitor of insulin-sensitive glucose transporters. Ischemic contracture during low-flow ischemia and creatine kinase release on reperfusion was decreased, and the percent recovery of left ventricular function with reperfusion was enhanced in hearts perfused with high glucose ( P < 0.03). Hearts perfused with high glucose exhibited increased GLUT-4 protein expression in the sarcolemmal membrane compared with control hearts under baseline conditions, and these changes were additive with low-flow ischemia. In addition, high glucose did not affect the baseline distribution of sarcolemmal GLUT-1 and blunted any changes with low-flow ischemia. These salutary effects were abolished when glucose transporters are blocked with cytochalasin B. These data demonstrate that protection of ischemic myocardium by high glucose is associated with increased sarcolemmal content of the insulin-sensitive GLUT-4 and suggest a target for the protection of jeopardized myocardium.

Glucose transport and transporters in muscle giant vesicles: differential effects of insulin and contractions

1993 ◽  
Vol 264 (2) ◽  
pp. E270-E278 ◽  
Author(s):  
T. Ploug ◽  
J. Wojtaszewski ◽  
S. Kristiansen ◽  
P. Hespel ◽  
H. Galbo ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Glucose Transport ◽  
Maximum Velocity ◽  
Enzyme Analysis ◽  
Marker Enzyme ◽  
Giant Vesicles ◽  
Western Blots ◽  
Glut 1 ◽  
Glut 4

Collagenase treatment of skeletal muscle results in the formation of large spheres of membranes (3–30 microns diam). A procedure is described for purification and concentration of these giant membrane vesicles prepared from rat muscle. Morphological observations, marker enzyme analysis, and immunoblotting demonstrate that the vesicles are of plasma membrane origin and that sarcoplasmic reticulum, T-tubules, and mitochondrial inner membranes are absent from the preparation. Western blots demonstrate that the vesicles contain GLUT-4 glucose transporters, whereas GLUT-1 could not be detected. Vesicles prepared from control muscle display specific transport of D-glucose with a maximum velocity (Vmax) for glucose influx of approximately 2,500 pmol.mg plasma membrane protein-1.s-1 and an apparent Michaelis constant (Km) of 16 mM measured at zero-trans conditions at room temperature. Muscle contractions in vivo doubled the Vmax of vesicle glucose transport and membrane GLUT-4 content but did not change Km. In contrast, in vivo administration of insulin did not affect vesicle glucose transport or membrane GLUT-4 content. The combination of insulin and contractions caused similar changes as did contractions alone. It is concluded that the present vesicle population contains membrane components almost exclusively derived from the plasma membrane and contains very little if any GLUT-1 but substantial amounts of GLUT-4. Thus the preparation allows the study of transport kinetics of pure GLUT-4 transporters. The procedure for preparing vesicles probably results in activation of the glucose transport system similar to the activation by insulin but not by contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of physical training on glucose transporter protein and mRNA levels in rat adipocytes

1993 ◽  
Vol 265 (1) ◽  
pp. E128-E134 ◽  
Author(s):  
B. Stallknecht ◽  
P. H. Andersen ◽  
J. Vinten ◽  
L. L. Bendtsen ◽  
J. Sibbersen ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Physical Training ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Intrinsic Activity ◽  
Mrna Levels ◽  
Glut 1 ◽  
Transporter Protein ◽  
Glut 4 ◽  
Adipocyte Volume

Physical training increases insulin-stimulated glucose transport and the number of glucose transporters in adipocytes measured by cytochalasin B binding. In the present study we used immunoblotting to measure the abundance of two glucose transporters (GLUT-4, GLUT-1) in white adipocytes from trained rats. Furthermore, the abundance of the mRNAs for these proteins and glucose transport was measured. Rats were swim-trained for 10 wk, and adipocytes were isolated from epididymal fat pads. The amount of GLUT-4/adipocyte volume unit was significantly higher in trained animals compared with both age- and cell size-matched animals. The amount of GLUT-4 mRNA was also increased by training and it decreased with increasing age. Furthermore, young age as well as training was accompanied by relatively low GLUT-4 protein/mRNA and relatively high overall GLUT-4 efficiency (recruitability and/or intrinsic activity). GLUT-1 protein and mRNA levels/adipocyte volume did not change with age or training.

Expression of glucose transporters (GLUT 1 and GLUT 4) in primary cultured rat adipocytes: Differential evolution with time and chronic insulin effect

1992 ◽  
Vol 49 (3) ◽  
pp. 251-258 ◽  
Author(s):  
Eric J. Hajduch ◽  
Michèle C. Guerre-Millo ◽  
Isabelle A. Hainault ◽  
Colette M. Guichard ◽  
Marcelle M. Lavau
Keyword(s):  
Differential Evolution ◽  
Glucose Transporters ◽  
Insulin Effect ◽  
Glut 1 ◽  
Rat Adipocytes ◽  
Glut 4 ◽  
Evolution With Time

Time-dependent and tissue-specific effects of circulating glucose on fetal ovine glucose transporters

1999 ◽  
Vol 276 (3) ◽  
pp. R809-R817 ◽  
Author(s):  
Utpala G. Das ◽  
Robert E. Schroeder ◽  
William W. Hay ◽  
Sherin U. Devaskar
Keyword(s):  
Skeletal Muscle ◽  
Gestational Age ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Time Dependent ◽  
Glut 1 ◽  
Glut 4 ◽  
Specific Effects ◽  
Glucose Transporter Proteins ◽  
Maternal Glucose

To determine the cellular adaptations to fetal hyperglycemia and hypoglycemia, we examined the time-dependent effects on basal (GLUT-1 and GLUT-3) and insulin-responsive (GLUT-4) glucose transporter proteins by quantitative Western blot analysis in fetal ovine insulin-insensitive (brain and liver) and insulin-sensitive (myocardium, skeletal muscle, and adipose) tissues. Maternal glucose infusions causing fetal hyperglycemia resulted in a transient 30% increase in brain GLUT-1 but not GLUT-3 levels and a decline in liver and adipose GLUT-1 and myocardial and skeletal muscle GLUT-1 and GLUT-4 levels compared with gestational age-matched controls. Maternal insulin infusions leading to fetal hypoglycemia caused a decline in brain GLUT-3, an increase in brain GLUT-1, and a subsequent decline in liver GLUT-1, with no significant change in insulin-sensitive myocardium, skeletal muscle, and adipose tissue GLUT-1 or GLUT-4 concentrations, compared with gestational age-matched sham controls. We conclude that fetal glucose transporters are subject to a time-dependent and tissue- and isoform-specific differential regulation in response to altered circulating glucose and/or insulin concentrations. These cellular adaptations in GLUT-1 (and GLUT-3) are geared toward protecting the conceptus from perturbations in substrate availability, and the adaptations in GLUT-4 are geared toward development of fetal insulin resistance.

Phosphatidylinositol 3-kinase and dynamics of insulin resistance in denervated slow and fast muscles in vivo

1997 ◽  
Vol 272 (4) ◽  
pp. E661-E670 ◽  
Author(s):  
J. S. Elmendorf ◽  
A. Damrau-Abney ◽  
T. R. Smith ◽  
T. S. David ◽  
J. Turinsky
Keyword(s):  
Insulin Receptor ◽  
Glucose Uptake ◽  
Soleus Muscle ◽  
Phosphatidylinositol 3 Kinase ◽  
Plantaris Muscle ◽  
Glut 1 ◽  
Glut 4 ◽  
Denervated Muscles ◽  
Phosphatidylinositol 3

Regulation of glucose uptake by 1- and 3-day denervated soleus (slow-twitch) and plantaris (fast-twitch) muscles in vivo was investigated. One day after denervation, soleus and plantaris muscles exhibited 62 and 65% decreases in insulin-stimulated 2-deoxyglucose uptake, respectively, compared with corresponding control muscles. At this interval, denervated muscles showed no alterations in insulin receptor binding and activity, amount and activity of phosphatidylinositol 3-kinase, and amounts of GLUT-1 and GLUT-4. Three days after denervation, there was no increase in 2-deoxyglucose uptake in response to insulin in soleus muscle, whereas plantaris muscle exhibited a 158% increase in basal and an almost normal absolute increment in insulin-stimulated uptake. Despite these differences, denervated soleus and plantaris muscles exhibited comparable decreases in insulin-stimulated activities of the insulin receptor (approximately 40%) and phosphatidylinositol 3-kinase (approximately 50%) and a pronounced decrease in GLUT-4. An increase in GLUT-1 in plantaris, but not soleus, muscle 3 days after denervation is consistent with augmented basal 2-deoxyglucose uptake in plantaris muscle at this interval. These results demonstrate that, in denervated muscles, there is a clear dissociation between insulin-stimulated 2-deoxyglucose uptake and upstream events involved in insulin-stimulated glucose uptake.

Stability of GLUT-1 and GLUT-4 expression in perfused rat muscle stimulated by insulin and exercise

1995 ◽  
Vol 78 (1) ◽  
pp. 46-52 ◽  
Author(s):  
X. X. Han ◽  
A. Handberg ◽  
L. N. Petersen ◽  
T. Ploug ◽  
H. Galbo
Keyword(s):  
Glucose Transporter ◽  
Glut 1 ◽  
Protein Levels ◽  
Glut 4 ◽  
Slow Twitch ◽  
Glucose Transporter Mrna ◽  
Fast Twitch ◽  
Transporter Expression

In vivo exercise and insulin may change the concentrations of GLUT-4 protein and mRNA in muscle. We studied in vitro whether adaptations in glucose transporter expression are initiated during a single prolonged period of contractions or during insulin stimulation. Rat hindquarters were perfused at 7 mM glucose for 2 h with or without insulin (> 20,000 microU/ml) while the sciatic nerve of one leg was stimulated to produce repeated tetanic contractions. During electrical stimulation, contraction force decreased 93 +/- 1% (SE; n = 26) and muscle glycogen was markedly diminished (P < 0.05). Both contractions and insulin markedly increased glucose transport and uptake (P < 0.05). At the end of contractions, glycogen was higher in the presence of than in the absence of insulin (24 +/- 4 vs. 14 +/- 3 mumol/g for the soleus and 13 +/- 2 vs. 8 +/- 1 mumol/g for the red gastrocnemius, respectively; P < 0.05). In nonstimulated muscle, glucose transporter mRNA and protein concentrations were higher in the soleus than in the white gastrocnemius (GLUT-4 mRNA 184 +/- 18 vs. 131 +/- 36 arbitrary units; GLUT-1 mRNA 173 +/- 29 vs. 114 +/- 26 arbitrary units; GLUT-4 protein 0.96 +/- 0.09 vs. 0.46 +/- 0.03 arbitrary units; GLUT-1 protein 0.41 +/- 0.08 vs. 0.19 +/- 0.05 arbitrary units, respectively; P < 0.05). These concentrations were not changed by contractions or insulin. In conclusion, GLUT-1 and GLUT-4 mRNA and protein levels are higher in slow-twitch oxidative than in fast-twitch glycolytic fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Transient Ischemia on the Expression of Glucose Transporters GLUT-1 and GLUT-4 in Rat Myocardium

1999 ◽  
Vol 31 (5) ◽  
pp. 1143-1155 ◽  
Author(s):  
Isabelle Tardy-Cantalupi ◽  
Christophe Montessuit ◽  
Irène Papageorgiou ◽  
Andréa Remondino-Müller ◽  
Françoise Assimacopoulos-Jeannet ◽  
...  
Keyword(s):  
Glucose Transporters ◽  
Rat Myocardium ◽  
Transient Ischemia ◽  
Glut 1 ◽  
Glut 4
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