Insulin-like effects of dithiothreitol on isolated rat adipocytes.
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.
D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D004229:Dithiothreitol / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism; D007700:Kinetics; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D011972:Receptor, Insulin / Q000187:drug effects
D007328:Insulin; D011972:Receptor, Insulin; D005947:Glucose; D004229:Dithiothreitol