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Research Article Free access | 10.1172/JCI105534

Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohydrate intolerance in Mild Diabetes Mellitus

Holbrooke S. Seltzer, E. William Allen, Arthur L. Herron Jr., and Mildred T. Brennan

Endocrinology Section, Veterans Administration Hospital, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas

†

Address requests for reprints to Dr. Holbrooke S. Seltzer, Veterans Administration Hospital, 4500 S. Lancaster Rd., Dallas, Texas 75216.

*

Submitted for publication September 13, 1965; accepted November 3, 1966.

This study was supported in part by research grant A-4708 from the National Institutes of Health and by a grant from the Upjohn Co., Kalamazoo, Mich.

This work was presented in part at the Forty-fifth Annual Session of the American College of Physicians, Atlantic City, N. J., on April 10, 1964.

Find articles by Seltzer, H. in: JCI | PubMed | Google Scholar

Endocrinology Section, Veterans Administration Hospital, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas

†

Address requests for reprints to Dr. Holbrooke S. Seltzer, Veterans Administration Hospital, 4500 S. Lancaster Rd., Dallas, Texas 75216.

*

Submitted for publication September 13, 1965; accepted November 3, 1966.

This study was supported in part by research grant A-4708 from the National Institutes of Health and by a grant from the Upjohn Co., Kalamazoo, Mich.

This work was presented in part at the Forty-fifth Annual Session of the American College of Physicians, Atlantic City, N. J., on April 10, 1964.

Find articles by Allen, E. in: JCI | PubMed | Google Scholar

Endocrinology Section, Veterans Administration Hospital, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas

†

Address requests for reprints to Dr. Holbrooke S. Seltzer, Veterans Administration Hospital, 4500 S. Lancaster Rd., Dallas, Texas 75216.

*

Submitted for publication September 13, 1965; accepted November 3, 1966.

This study was supported in part by research grant A-4708 from the National Institutes of Health and by a grant from the Upjohn Co., Kalamazoo, Mich.

This work was presented in part at the Forty-fifth Annual Session of the American College of Physicians, Atlantic City, N. J., on April 10, 1964.

Find articles by Herron, A. in: JCI | PubMed | Google Scholar

Endocrinology Section, Veterans Administration Hospital, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas

†

Address requests for reprints to Dr. Holbrooke S. Seltzer, Veterans Administration Hospital, 4500 S. Lancaster Rd., Dallas, Texas 75216.

*

Submitted for publication September 13, 1965; accepted November 3, 1966.

This study was supported in part by research grant A-4708 from the National Institutes of Health and by a grant from the Upjohn Co., Kalamazoo, Mich.

This work was presented in part at the Forty-fifth Annual Session of the American College of Physicians, Atlantic City, N. J., on April 10, 1964.

Find articles by Brennan, M. in: JCI | PubMed | Google Scholar

Published March 1, 1967 - More info

Published in Volume 46, Issue 3 on March 1, 1967
J Clin Invest. 1967;46(3):323–335. https://doi.org/10.1172/JCI105534.
© 1967 The American Society for Clinical Investigation
Published March 1, 1967 - Version history
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Abstract

Insulin secretory responses to paired intravenous and oral glucose loads were determined in 38 nonobese individuals classified as normal (nondiabetic) subjects, “mild” diabetics (fasting blood glucose below 105 mg per 100 ml), or “moderate” diabetics (fasting glucose below 192 mg per 100 ml). Studies were also performed in 29 obese persons who were similarly grouped. The intravenous load was given to assess the alacrity of hormonal release after glycemic stimulus, and the oral glucose to determine how the speed of initial insulinogenesis modifies the disposition of ingested carbohydrate.

In the nonobese group, normal subjects responded to massive hyperglycemia after rapid injection of glucose with immediate and maximal outpouring of insulin, in contrast to a desultory insulinogenic response in patients with mild diabetes, and no initial response at all in moderate diabetics. During oral glucose tolerance tests, the much faster clearance of blood sugar in nondiabetic subjects was actually associated with lower absolute insulin output than was found in mildly diabetic patients, since the latter exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia. Moderate diabetics never showed excessive insulin release despite even greater hyperglycemia. An empirical “insulinogenic index,” the ratio relating enhancement of circulating insulin to magnitude of corresponding glycemic stimulus, was used to compare the secretory capacities of respective groups. Despite the higher absolute hormonal output after oral glucose in mild diabetics, the index revealed that insulin release in normal subjects was proportionally more than twice as great. This relatively greater normal secretory response declared itself shortly after the administration of glucose by either route, and was maintained throughout both tests.

In the 29 obese individuals, differences among groups were essentially the same as in persons of normal weight. Obese nondiabetics did show much larger absolute insulinogenic responses during both tests than did nonobese controls. Since corresponding glucose tolerance curves were also higher, the mean insulinogenic indexes for obese subjects were not statistically greater. Moreover, when comparable glucose curves of obese and nonobese controls

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