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Glucose Intolerance and Insulin Resistance in Patients With Liver DiseaseII. A Study of Etiologic Factors and Evaluation of Insulin Actions
John R. Collins, MD;
William W. Lacy, MD;
John N. Stiel, MB;
Oscar B. Crofford, MD
Arch Intern Med. 1970;126(4):608-614.
Abstract
A study of patients with compensated liver disease revealed (1) inappropriately high serum insulin levels in response to a glucose load administered either orally or intravenously, and (2) a diminished glucose response to injected insulin. These observations suggested "resistance" to the regulatory action of insulin on glucose metabolism. The actions of insulin on fat and protein metabolism, as reflected by lowering of free fatty acid (FFA) and free amino acid levels after glucose loads, were not altered. Since disappearance of injected insulin proceeded at a normal rate, insulin hypersecretion, as opposed to reduced insulin degradation, was suggested as the cause of the hyperinsulinemia. Potassium depletion, FFA elevation, and elevation of growth hormone levels could not be implicated as the cause of the abnormalities noted.
Author Affiliations
Nashville, Tenn
From the Department of Medicine, Vanderbilt University School of Medicine and Veterans Administration Hospital, Nashville, Tenn.
Footnotes
Received for publication Dec 29, 1969; accepted March 16,1970.
Reprint requests to A-5119, Vanderbilt Medical Center, Nashville, Tenn 37203 (Dr. Collins).
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