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Clinical Research Unit and the Department of Medicine, University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania the Diabetes Research Laboratory, St. Luke's Episcopal Hospital, Baylor College of Medicine Houston, Texas 77025
Address requests for reprints to: Dr. James B. Field, Division of Endocrinology/Metabolism, St. Luke's Episcopal Hospital, Baylor College of Medicine, P.O. Box 20269, Houston, Texas 77025.
The effect of increasing caloric intake on blood glucose regulation was investigated in nine mild, adult-onset diabetic patients treated by diet with or without oral hriypoglycemic agents. During the initial week of hospitalization, patients received their previously prescribed diet and oral hypoglycemic agents. Blood sugar and plasma insulin was determined before each meal, and 24-h glycosuria was quantitated. The diet was then increased by 500 cal/day each week until the basal calories doubled or the patient could not consume the additional food. The percentage distribution among carbohydrate, protein, and fat and feedings during the day were kept constant. In four of the patients, no significant increase in blood glucose was observed despite the doubling of caloric intake. In an additional four patients, only one of the four blood glucose determinations was significantly increased as a consequence of the increased calories. The plasma insulin values in six of these patients demonstrated significant increases in association with the higher caloric intake. In two patients, no change in plasma insulin was observed despite the lack of deterioration of the blood glucose values. The ninth patient had significant elevation of all of the four blood> sugar values in association with the increased caloric intake. In this patient, the hyperglycemia was not accompanied by any change in the plasma insulin levels.
The results indicate that during short periods of increased caloric intake, mild diabetic patients are able to prevent deterioration of their diabetic regulation by increasing either their insulin secretion or their sensitivity to the hormone. The data are compatible with the existence of an elevated threshold for insulin release in response to glucose in such patients.
* This work was supported by USPHS Grant AM-25253 and Clinical Research Center Grant RR-56.
Received April 10, 1979.
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