The relationship between the transport of glucose and cations across cell membranes in isolated tissues. IX. The role of cellular calcium in the activation of the glucose transport system in rat soleus muscle

1975 ◽  
Vol 375 (2) ◽  
pp. 292-308 ◽  
Author(s):  
T. Clausen ◽  
J. Elbrink ◽  
A.B. Dahl-Hansen
Keyword(s):  
Glucose Transport ◽  
Transport System ◽  
Soleus Muscle ◽  
Cell Membranes ◽  
Cellular Calcium ◽  
Glucose Transport System ◽  
Rat Soleus Muscle ◽  
The Relationship ◽  
Isolated Tissues

Effects of insulin and epinephrine on Na+-K+ and glucose transport in soleus muscle

1987 ◽  
Vol 252 (4) ◽  
pp. E492-E499 ◽  
Author(s):  
T. Clausen ◽  
J. A. Flatman
Keyword(s):  
Glucose Transport ◽  
Soleus Muscle ◽  
Sugar Transport ◽  
Resting Membrane Potential ◽  
Exchange System ◽  
Glucose Transport System ◽  
Rat Soleus Muscle ◽  
Possible Cause ◽  
K Transport ◽  
Stimulation Of

To identify possible cause-effect relationships between changes in active Na+-K+ transport, resting membrane potential, and glucose transport, the effects of insulin and epinephrine were compared in rat soleus muscle. Epinephrine, which produced twice as large a hyperpolarization as insulin, induced only a modest increase in sugar transport. Ouabain, at a concentration (10(-3) M) sufficient to block active Na+-K+ transport and the hyperpolarization induced by the two hormones, did not interfere with sugar transport stimulation. After Na+ loading in K+-free buffer, the return to K+-containing standard buffer caused marked stimulation of active Na+-K+ transport, twice the hyperpolarization produced by insulin but no change in sugar transport. The insulin-induced activation of the Na+-K+ pump leads to decreased intracellular Na+ concentration and hyperpolarization, but none of these events can account for the concomitant activation of the glucose transport system. The stimulating effect of insulin on active Na+-K+ transport was not suppressed by amiloride, indicating that in intact skeletal muscle it is not elicited by a primary increase in Na+ influx via the Na+/H+-exchange system.

scholarly journals In vitro analysis of the glucose-transport system in GLUT4-null skeletal muscle

1999 ◽  
Vol 342 (2) ◽  
pp. 321-328 ◽  
Author(s):  
Jeffrey W. RYDER ◽  
Yuichi KAWANO ◽  
Alexander V. CHIBALIN ◽  
Jorge RINCÓN ◽  
Tsu-Shuen TSAO ◽  
...  
Keyword(s):  
Cell Surface ◽  
Glucose Transport ◽  
Transport System ◽  
Soleus Muscle ◽  
Cytochalasin B ◽  
Transport Activity ◽  
Wild Type ◽  
Glucose Transport System ◽  
Vitro Analysis

We have characterized the glucose-transport system in soleus muscle from female GLUT4-null mice to determine whether GLUT1, 3 or 5 account for insulin-stimulated glucose-transport activity. Insulin increased 2-deoxyglucose uptake 2.8- and 2.1-fold in soleus muscle from wild-type and GLUT4-null mice, respectively. Cytochalasin B, an inhibitor of GLUT1- and GLUT4-mediated glucose transport, inhibited insulin-stimulated 2-deoxyglucose uptake by > 95% in wild-type and GLUT4-null soleus muscle. Addition of 35 mM fructose to the incubation media was without effect on insulin-stimulated 3-O-methylglucose transport activity in soleus muscle from either genotype, whereas 35 mM glucose inhibited insulin-stimulated (20 nM) 3-O-methylglucose transport by 65% in wild-type and 99% in GLUT4-null mice. We utilized the 2-N-4-1-(1-azi-2,2,2-t r i f l u o r o e t h y l ) b e n z o y l - 1, 3 - b i s (D - m a n n o s e - 4 - y l o x y ) - 2 - p ro p y lamine (ATB-BMPA) exofacial photolabel to determine if increased cell-surface GLUT1 or GLUT4 content accounted for insulin-stimulated glucose transport in GLUT4-null muscle. In wild-type soleus muscle, cell-surface GLUT4 content was increased by 2.8-fold under insulin-stimulated conditions and this increase corresponded to the increase in 2-deoxyglucose uptake. No detectable cell-surface GLUT4 was observed in soleus muscle from female GLUT4-null mice under either basal or insulin-stimulated conditions. Basal cell-surface GLUT1 content was similar between wild-type and GLUT4-null mice, with no further increase noted in either genotype with insulin exposure. Neither GLUT3 nor GLUT5 appeared to account for insulin-stimulated glucose-transport activity in wild-type or GLUT4-null muscle. In conclusion, insulin-stimulated glucose-transport activity in female GLUT4-null soleus muscle is mediated by a facilitative transport process that is glucose- and cytochalasin B-inhibitable, but which is not labelled strongly by ATB-BMPA.

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