Walter A. Müller, … , Gerald R. Faloona, Roger H. Unger
Citation Information: J Clin Invest. 1971;50(9):1992-1999. https://doi.org/10.1172/JCI106691.
Walter A. Müller, … , Gerald R. Faloona, Roger H. Unger
Published September 1, 1971
Citation Information: J Clin Invest. 1971;50(9):1992-1999. https://doi.org/10.1172/JCI106691.
Abstract
Suppression of pancreatic glucagon secretion by hyperglycemia is a characteristic of normal alpha cell function. However, in diabetic subjects, plasma glucagon is normal or high despite hyperglycemia. It seemed possible that the presence of glucose or its metabolites within the alpha cell might be essential for suppression of glucagon secretion, and that in diabetes an intracellular deficiency of glucose secondary to insulin lack might be responsible for the nonsuppressibility. The present study was designed to determine the effect upon glucagon secretion of blockade of glucose metabolism and of experimental insulin deficiency.
Authors
Walter A. Müller, Gerald R. Faloona, Roger H. Unger
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