Plasma insulin responses to glucose and tolbutamide of normal weight and obese diabetic and nondiabetic subjects
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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These individuals have a defect in β-cell response to intravenous secretagogues including glucose.
“these individuals manifest a defect in the ability of the islet β-cell to respond to intravenous secretagogues including glucose3.”
From Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future (2014) · cites this paper as [3]
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- 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
- 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 › Surgery › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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