scholarly journals Effects of fasting on insulin binding, glucose transport, and glucose oxidation in isolated rat adipocytes: relationships between insulin receptors and insulin action.

1976 ◽  
Vol 58 (6) ◽  
pp. 1450-1460 ◽  
Author(s):  
J M Olefsky
1982 ◽  
Vol 4 (4) ◽  
pp. 261-271 ◽  
Author(s):  
Tj. Wieringa ◽  
G. Bruin ◽  
W. P. M. Meerwijk ◽  
H. M. J. Krans

1982 ◽  
Vol 14 (4) ◽  
pp. 261-271
Author(s):  
Tj. Wieringa ◽  
G. de Bruin ◽  
W. P. M. van Meerwijk ◽  
H. M. J. Krans

1981 ◽  
Vol 200 (2) ◽  
pp. 425-428 ◽  
Author(s):  
H Goko ◽  
S Takashima ◽  
A Kawamuro ◽  
A Matsuoka

The effects of dithiothreitol on basal glucose oxidation, hormone-induced lipolysis and insulin receptors in isolated rat adipocytes were studied. Dithiothreitol produced a dose-dependent stimulation of basal glucose oxidation and inhibition of adrenaline-induced lipolysis. Dithiothreitol also inhibited corticotropin-induced lipolysis, but failed to inhibit dibutyryl cyclic AMP-induced lipolysis. Dithiothreitol did not inhibit the binding of the beta-adrenergic antagonist [3H]dihydroalprenolol to adipocytes. Neither catalase (100 micrograms/ml) nor EDTA (2 mM) abolished the antilipolytic effect of dithiothreitol. Treatment of isolated adipocytes with 1 mM-dithiothreitol for 20 min at 37 degrees C also caused stimulation of basal glucose oxidation and inhibition of adrenaline-induced lipolysis. A Scatchard plot of insulin binding to control adipocytes was curvilinear. However, treatment of cells with 1 mM-dithiothreitol decreased the curvilinearity of the plot, indicating that only a low-affinity state of the insulin receptors exists in the dithiothreitol-treated adipocytes. These findings suggest that the insulin-like activities of dithiothreitol are mediated through the interaction of dithiothreitol with insulin receptors.


1992 ◽  
Vol 70 (8) ◽  
pp. 1190-1194 ◽  
Author(s):  
Nirmal S. Basi ◽  
K. G. Thomaskutty ◽  
Richard H. Pointer

When isolated rat adipocytes were incubated with increasing concentrations of levamisole (0.5–5 mM), basal glucose oxidation decreased by almost 50% and insulin-stimulated glucose oxidation decreased by 90%. The decrease in glucose oxidation correlated with an inhibition of glucose transport, since levamisole at 5.0 mM decreased basal 3-O-methylglucose transport by 60% and insulin-stimulated transport by 80%. Diamide-stimulated glucose transport was also inhibited approximately 80% by 5.0 mM levamisole. Levamisole at concentrations up to 5.0 mM had no effect on phosphofructokinase activity. The present results suggest that levamisole inhibits glucose utilization by inhibiting glucose transport in a concentration-dependent manner.Key words: insulin, levamisole, glucose transport, adipocytes.


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