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Research Article Free access | 10.1172/JCI107692

Adrenergic Modulation of Pancreatic Glucagon Secretion in Man

John E. Gerich, Maurice Langlois, Claudio Noacco, Victor Schneider, and Peter H. Forsham

1Metabolic Research Unit and Department of Medicine, University of California, San Francisco, California 94143

Find articles by Gerich, J. in: PubMed | Google Scholar

1Metabolic Research Unit and Department of Medicine, University of California, San Francisco, California 94143

Find articles by Langlois, M. in: PubMed | Google Scholar

1Metabolic Research Unit and Department of Medicine, University of California, San Francisco, California 94143

Find articles by Noacco, C. in: PubMed | Google Scholar

1Metabolic Research Unit and Department of Medicine, University of California, San Francisco, California 94143

Find articles by Schneider, V. in: PubMed | Google Scholar

1Metabolic Research Unit and Department of Medicine, University of California, San Francisco, California 94143

Find articles by Forsham, P. in: PubMed | Google Scholar

Published May 1, 1974 - More info

Published in Volume 53, Issue 5 on May 1, 1974
J Clin Invest. 1974;53(5):1441–1446. https://doi.org/10.1172/JCI107692.
© 1974 The American Society for Clinical Investigation
Published May 1, 1974 - Version history
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Abstract

In order to characterize the influence of the adrenergic system on pancreatic glucagon secretion in man, changes in basal glucagon secretion during infusions of pure alpha and beta adrenergic agonists and their specific antagonists were studied. During infusion of isoproterenol (3 μg/min), a beta adrenergic agonist, plasma glucagon rose from a mean (±SE) basal level of 104±10 to 171±15 pg/ml, P < 0.0002. Concomitant infusion of propranolol (80 μg/min), a beta adrenergic antagonist, prevented the effects of isoproterenol, although propranolol itself had no effect on basal glucagon secretion. During infusion of methoxamine (0.5 mg/min), an alpha adrenergic agonist, plasma glucagon declined from a mean basal level of 122±15 to 75±17 pg/ml, P < 0.001. Infusion of phentolamine (0.5 mg/min), an alpha adrenergic antagonist, caused a rise in plasma glucagon from a mean basal level of 118±16 to 175±21 pg/ml, P < 0.0001. Concomitant infusion of methoxamine with phentolamine caused a reversal of the effects of phentolamine.

The present studies thus confirm that catecholamines affect glucagon secretion in man and demonstrate that the pancreatic alpha cell possesses both alpha and beta adrenergic receptors. Beta adrenergic stimulation augments basal glucagon secretion, while alpha adrenergic stimulation diminishes basal glucagon secretion. Furthermore, since infusion of phentolamine, an alpha adrenergic antagonist, resulted in an elevation of basal plasma glucagon levels, there appears to be an inhibitory alpha adrenergic tone governing basal glucagon secretion. The above findings suggest that catecholamines may influence glucose homeostasis in man through their effects on both pancreatic alpha and beta cell function.

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