Toxic effects of glucagon-induced acute lipid mobilization in geese

John C. Hoak; William E. Connor; Emory D. Warner

doi:10.1172/JCI105953

^{Cardiovascular Research Laboratories, the Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

^{Cardiovascular Research Laboratories, the Department of Pathology, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

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^{Cardiovascular Research Laboratories, the Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

^{Cardiovascular Research Laboratories, the Department of Pathology, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

Find articles by Connor, W. in: JCI | PubMed | Google Scholar

^{Cardiovascular Research Laboratories, the Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

^{Cardiovascular Research Laboratories, the Department of Pathology, University of Iowa, College of Medicine, Iowa City, Iowa 52240}

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Published in Volume 47, Issue 12 on December 1, 1968
J Clin Invest. 1968;47(12):2701–2710. https://doi.org/10.1172/JCI105953.
© 1968 The American Society for Clinical Investigation

Published December 1, 1968 - Version history

The toxic effects associated with rapid lipid mobilization and a high plasma free fatty acid (FFA) concentration produced by glucagon were evaluated. Glucagon (0.5 mg/kg of body wt) was injected intravenously into nonfasting geese. The geese developed rapid respirations and high plasma FFA levels within 15 min after the glucagon injection; three of eleven died. Control geese, injected with saline, did not exhibit toxic signs. Peak FFA concentrations developed 15 min after glucagon and high levels persisted for over 90 min. Geese injected with glucagon frequently developed electrocardiographic abnormalities that included supraventricular tachycardia, premature ventricular contractions, and signs of myocardial ischemia. Light and electron microscopy revealed acute myocardial degeneration and fatty infiltration of the liver. The increase in plasma FFA concentrations and toxic effects were not prevented by pretreatment with nicotinic acid or propranolol.

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