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AJP - Endocrinology and Metabolism, Vol 261, Issue 6 E764-E772, Copyright © 1991 by American Physiological Society
ARTICLES |
C. C. Connolly, K. E. Steiner, R. W. Stevenson, D. W. Neal, P. E. Williams, K. G. Alberti and A. D. Cherrington
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
The effects of norepinephrine (NE) at levels present in the circulation and synaptic cleft during stress on glucose metabolism were examined in overnight-fasted conscious dogs with fixed basal levels of insulin and glucagon. Plasma NE rose from 132 +/- 14 to 442 +/- 85 pg/ml and 100 +/- 20 to 3,244 +/- 807 pg/ml during 3 h of low (n = 6) and high (n = 5) NE infusion, respectively. Plasma glucose and glucose production rose only with high NE infusion (from 108 +/- 4 to 159 +/- 15 mg/dl and 2.78 +/- 0.24 to 3.41 +/- 0.38 mg.kg-1.min-1, respectively). NE infusion caused dose-dependent net hepatic lactate consumption, but net hepatic alanine uptake fell only with high NE infusion (31%). Alanine conversion to glucose rose by 67 +/- 13, 136 +/- 20, and 412 +/- 104%, and intrahepatic gluconeogenic efficiency rose by 42 +/- 27, 299 +/- 144, and 212 +/- 21% with saline and with low and high NE infusion, respectively. In conclusion, NE enhances gluconeogenesis by stimulating peripheral precursor release, by increasing substrate movement into the hepatocyte, and by increasing intrahepatic gluconeogenic efficiency. However, only the higher NE levels affected glucose metabolism profoundly enough to stimulate glucose production and to elevate the glucose level.
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