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Journal of Lipid Research, Vol. 9, 714-719, November 1968
New England Medical Center Hospitals and Department of Medicine, Tufts University School of Medicine, and The Department of Physiology, Harvard Medical School, Boston, Massachusetts 02111
Epinephrine increases the oxidation of glucose in adipose tissue even when its lipolytic effects are markedly reduced or abolished by propranolol, nicotinic acid, ouabain, or thyroidectomy. In order to locate the site(s) at which epinephrine stimulates glucose utilization, we studied the effects of epinephrine on the oxidation of various metabolites of glucose. Epinephrine neither increased the production of 14CO2 from 1- or 3-14C-pyruvate nor affected pyruvate conversion to glyceride-glycerol. To assess the possibility that epinephrine might accelerate the entry of glucose into adipocytes, we studied the accumulation of the nonmetabolized sugar l-arabinose in the intracellular water of adipose tissue. Epinephrine increased arabinose penetration into adipocytes to a degree comparable with that caused by 0.1 mU/ml of insulin. Virtually identical results were obtained in tissues from thyroidectomized rats in which the lipolytic effects of epinephrine were significantly reduced. It is concluded that epinephrine increases glucose oxidation by promoting its entry into adipose tissue and that the effect is independent of lipolysis. Supplementary key words lipolysis glucose oxidation ouabain propranolol nicotinic acid insulin l-arabinose
Submitted on March 25, 1968
Copyright © 1968 by Lipid Research, Inc.
Effects of epinephrine on glucose transport and metabolism in adipose tissue of normal and hypothyroid rats
Accepted on July 29, 1968
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