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Cited by 330Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes Management and Research

The DOI matches its Crossref record.

Plasma Insulin Responses to Glucose and Tolbutamide of Normal Weight and Obese Diabetic and Nondiabetic Subjects

Perley, Michael, Kipnis, David M·1966·Diabetes
DOI 10.2337/diab.15.12.867
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Abstract

Plasma insulin responses to oral glucose (100 gm.) and intravenous tolbutamide (1.0 gm.) before and after dexamethasone were determined in normal, obese nondiabetic, normal-weight diabetic and obese diabetic subjects. Fasting plasma insulin levels were significantly higher in obese nondiabetic and obese diabetic subjects than in normalweight nondiabetic and diabetic individuals. Total plasma insulin response to oral glucose in obese nondiabetics was threefold greater, in obese diabetic 2.2-fold greater, and in normal-weight diabetics 1.7-fold greater than that observed in normal individuals. When the plasma insulin responses of obese diabetic and nondiabetic subjects were measured at comparable blood sugar levellN insulin secretion was demonstrated to be significantly impaired in the diabetic group. The initial plasma insulin response (i.e., thirty-minute level) to glucose of diabetic subjects is markedly impaired when compared to normal-weight and obese nondiabetic individuals. Total plasma insulin response to intravenous tolbutamide was fourfold greater in obese nondiabetic and obese diabetic subjects than in normal-weight nondiabetic and diabetic individuals. Following dexamethasone (2 mg. q.i.d. × 2), plasma insulin response to intravenous tolbutamide was increased fivefold in normal subjects, threefold in obese nondiabetics, 1.6-fold in obese diabetics and twofold in nonobese diabetics. The results of these studies indicate that obesity is associated with a hypersecretory insulin response to both tolbutamide and glucose. The presence of overt diabetes melitus indicates an impairment in insulin response in both obese and nonobese individuals when compared to their appropriate nondiabetic controls. Dexamethasone provokes a marked compensatory insulin response in nondiabetics and makes more apparent the impaired secretory capacity of diabetic subjects. Maturity-onset diabetes in nonobaese individuals appears to be a consequence primarily of insulin deficiency. In obese diabetic individuals, however, even though secretory capacity may be significantly greater than observed in nonobese diabetics, impaired carbohydrate tolerance develops because insulin antagonism associated with obesity per se.

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Metadata

Authors
Perley, M., & Kipnis, D. M.
Affiliations
Washington University in St. Louis (US)
Venue
Diabetes
Publisher
American Diabetes Association
Published
1966-12-01
Volume
15
Issue
12
Pages
867-874
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.15.12.867
OpenAlex
W2083606604
Cited by
330
References
0
Citations by year
2024: 1 · 2023: 1 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 4 · 2017: 7 · 2016: 4 · 2015: 4 · 2014: 3 · 2013: 7 · 2012: 3
FWCI
56.09
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Keywords
plasma insulin response, obesity, type 2 diabetes, oral glucose tolerance, tolbutamide, dexamethasone, insulin secretion, insulin resistance, insulin deficiency, carbohydrate tolerance, insulin antagonism
MeSH terms
Dexamethasone, Diabetes Mellitus, Fasting, Glucose, Humans, Injections, Intravenous, Insulin, Obesity, Tolbutamide

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