The Significance of Basal Insulin Levels in the Evaluation of the Insulin Response to Glucose in Diabetic and Nondiabetic Subjects (original) (raw)
Research Article Free access | 10.1172/JCI105646
Department of Medicine, University of Washington School of Medicine, and the Veterans Administration Hospital, Seattle, Washington
‡
Assistant in Medicine, University of Washington School of Medicine; Postdoctoral Research Fellow, National Institutes of Health.
§
Associate Professor of Medicine, University of Washington School of Medicine; Chief, Metabolic Disease Service, VA Hospital, Seattle; Career Development Awardee, 5K3 AM-28, 167, National Institutes of Health.
ǁ
Assistant Professor of Medicine, University of Washington School of Medicine; Clinical Investigator, VA Hospital, Seattle.
*
Received for publication 17 March 1967 and in revised form 9 June 1967.
Supported in part by U. S. Public Health Service Grant AM-06670. A portion of this work was conducted through the Clinical Research Center facility of the University of Washington (NIH Grant FR-37). Presented in part at the 20th Annual Meeting of the Western Society for Clinical Research, Carmel, Calif., 26 January 1967. (1967. Clin. Res. 15: 137).
Find articles by Bagdade, J. in:[JCI](/search/results?q=author.first%5Fname%3A%22John D.%22+author.last%5Fname%3A%22Bagdade%22&search%5Ftype=advanced) |PubMed |Google Scholar
Department of Medicine, University of Washington School of Medicine, and the Veterans Administration Hospital, Seattle, Washington
‡
Assistant in Medicine, University of Washington School of Medicine; Postdoctoral Research Fellow, National Institutes of Health.
§
Associate Professor of Medicine, University of Washington School of Medicine; Chief, Metabolic Disease Service, VA Hospital, Seattle; Career Development Awardee, 5K3 AM-28, 167, National Institutes of Health.
ǁ
Assistant Professor of Medicine, University of Washington School of Medicine; Clinical Investigator, VA Hospital, Seattle.
*
Received for publication 17 March 1967 and in revised form 9 June 1967.
Supported in part by U. S. Public Health Service Grant AM-06670. A portion of this work was conducted through the Clinical Research Center facility of the University of Washington (NIH Grant FR-37). Presented in part at the 20th Annual Meeting of the Western Society for Clinical Research, Carmel, Calif., 26 January 1967. (1967. Clin. Res. 15: 137).
Find articles by Bierman, E. in:[JCI](/search/results?q=author.first%5Fname%3A%22Edwin L.%22+author.last%5Fname%3A%22Bierman%22&search%5Ftype=advanced) |PubMed |Google Scholar
Department of Medicine, University of Washington School of Medicine, and the Veterans Administration Hospital, Seattle, Washington
‡
Assistant in Medicine, University of Washington School of Medicine; Postdoctoral Research Fellow, National Institutes of Health.
§
Associate Professor of Medicine, University of Washington School of Medicine; Chief, Metabolic Disease Service, VA Hospital, Seattle; Career Development Awardee, 5K3 AM-28, 167, National Institutes of Health.
ǁ
Assistant Professor of Medicine, University of Washington School of Medicine; Clinical Investigator, VA Hospital, Seattle.
*
Received for publication 17 March 1967 and in revised form 9 June 1967.
Supported in part by U. S. Public Health Service Grant AM-06670. A portion of this work was conducted through the Clinical Research Center facility of the University of Washington (NIH Grant FR-37). Presented in part at the 20th Annual Meeting of the Western Society for Clinical Research, Carmel, Calif., 26 January 1967. (1967. Clin. Res. 15: 137).
Find articles by Porte, D. in:JCI |PubMed |Google Scholar
Published October 1, 1967 -More info
Published October 1, 1967 -Version history
The level of insulin after an overnight fast (basal) in 37 obese and nonobese male subjects with normal and abnormal carbohydrate tolerance was directly related to the increase in insulin concentration during a 3 hr 100 g oral glucose tolerance test. Obesity, but not diabetes, was associated with an elevation of this basal insulin level. Thus obesity predicted with the magnitude of the insulin response to glucose ingestion. When the individual insulin values were expressed as per cent change from the basal level, this effect of obesity was excluded. The insulin levels of all subjects with normal carbohydrate tolerance promptly rose 5-7-fold, and reached peak values 1 hr after oral glucose. In contrast, the diabetic response (as per cent increase) was markedly reduced during the 1st hr, and maximal (but still subnormal) insulin levels were not attained until 2 hr. In all subjects the insulin response (quantitated by calculation of the area circumscribed by a plot of the per cent change in insulin with time) showed a significant inverse correlation with the glucose response. Thus increasing degrees of carbohydrate intolerance were associated with decreasing insulin responses. Elevated levels of insulin, in both the basal state and in response to glucose, were related to obesity.
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