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Abnormal Pancreatic Glucagon Secretion and Postprandial Hyperglycemia In Diabetes Mellitus
John E. Gerich, MD;
Mara Lorenzi, MD;
John H. Karam, MD;
Victor Schneider, MD;
Peter H. Forsham, MD
JAMA. 1975;234(2):159-165.
Abstract
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Plasma glucose and glucagon responses to standard meals containing carbohydrate, fat, and protein as in normal diets were studied in 12 subjects with insulin-dependent diabetes and 12 normal subjects. Diabetics had two to three times greater glucagon responses than did normal subjects. Fifteen units of insulin injection did not normalize these excessive glucagon responses, although postprandial hyperglycemia was reduced. Infusion of somatostatin at a dosage of 500µg/hr prevented glucagon responses and diminished postprandial hyperglycemia by 60%. The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia.
These studies indicate that excessive glucagon secretion participates in the genesis of diabetic postprandial hyperglycemia. Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus.
(JAMA 234:159-165, 1975)
Author Affiliations
From the Metabolic Research Unit (Drs. Gerich, Karam, and Forsham) and the Department of Medicine, University of California, San Francisco.
Footnotes
Reprint requests to Metabolic Research Unit, 1143 HSW, University of California, San Francisco, CA 94143 (Dr. Gerich).
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