Plasma Insulin Responses to Oral and Intravenous Glucose: Studies in Normal and Diabetic Subjects*
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The plasma insulin responses of normal weight and obese, diabetic, and nondiabetic subjects to intravenous glucose was only 30-40% of that seen after oral glucose, indicating that alimentary mechanism(s) in addition to the arterial blood sugar concentration regulate insulin secretion. Observations made in subjects with diverted portal circulation indicate that the alimentary insulinogenic mechanism is located in the intestinal tract. The insulinogenic potency of the alimentary and glycemic stimuli expressed in terms of insulin secretion per gram of glucose were remarkably similar within each group of individuals. Between these groups, however, there were considerable differences. Obesity, with or without associated diabetes, was associated with a true hypersecretory responsiveness, whereas diabetes was characterized, with or without obesity, by a marked impairment in insulin secretion. The experimental design used in these studies permitted quantitation of the magnitude of the glycemic component of an oral glucose load. As a consequence of impaired insulin secretion, a greater than normal proportion of the oral glucose load escapes initial hepatic extraction in the maturity-onset diabetic and enters the peripheral circulation. Therefore, in the noninsulin-requiring maturity-onset diabetic, the glycemic insulinogenic stimulus for a given oral glucose load is significantly greater than in normal subjects and accounts for the excessive plasma insulin responses observed late in the course of an oral glucose tolerance test.
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Obesity and its associated insulin resistance are associated with basal and stimulated hyperinsulinaemia.
“obesity and its associated insulin resistance are associated with basal and stimulated hyperinsulinaemia [10, 68, 91, 92].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [68]
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RetractedGIP and GLP-1 as incretin hormones: lessons from single and double incretin receptor knockout mice
Hansotia, T., & Drucker, D. J. (2004) · Regulatory Peptides · doi:10.1016/j.regpep.2004.07.019 · Cited by 182 · see citing works
The Macronutrients, Appetite, and Energy Intake
Carreiro, A. L., Dhillon, J., Gordon, S. L., Higgins, K., Jacobs, A., McArthur, B. M., Redan, B. W., Rivera, R. L., Schmidt, L. R., & Mattes, R. D. (2016) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-121415-112624 · Cited by 182 · see citing works
Power, O., Nongonierma, A. B., Jakeman, P. M., & Fitzgerald, R. J. (2013) · Proceedings of The Nutrition Society · doi:10.1017/s0029665113003601 · Cited by 181 · see citing works
Gut hormones and diabetes mellitus
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First-phase insulin secretion: does it exist in real life? Considerations on shape and function
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Interactions between kidney disease and diabetes: dangerous liaisons
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Cholesterol in islet dysfunction and type 2 diabetes
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Regulation of hepatic glucose metabolism in humans
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The Effect of Gastrin on Basal- and Glucose-Stimulated Insulin Secretion in Man
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Plasma triglyceride response to carbohydrates, fats and caloric intake
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Comparative Clinical Pharmacokinetics of Dipeptidyl Peptidase-4 Inhibitors
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DPP-4 inhibitors for treating T2DM - hype or hope? an analysis based on the current literature
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Effect of diet composition on the hyperinsulinemia of obesity
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Self-citationBeta cell mass in diabetes: a realistic therapeutic target?
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Plasma glucose and insulin response to macronutrients in nondiabetic and NIDDM subjects
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- Authors
- Perley, M. J., & Kipnis, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1967-12-01
- Volume
- 46
- Issue
- 12
- Pages
- 1954-1962
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC292948
- OpenAlex
- W2169558934
- Cited by
- 917
- References
- 24
- Citations by year
- 2026: 12 · 2025: 12 · 2024: 15 · 2023: 17 · 2022: 12 · 2021: 16 · 2020: 20 · 2019: 25 · 2018: 15 · 2017: 15 · 2016: 28 · 2015: 33 · 2014: 13 · 2013: 25 · 2012: 16
- FWCI
- 60.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- insulin secretion, oral glucose tolerance, intravenous glucose, obesity, type 2 diabetes, hypersecretion, insulin resistance
- MeSH terms
- Adolescent, Adult, Aged, Arteries, Capillaries, Child, Diabetes Mellitus, Glucose, Humans, Infusions, Parenteral, Insulin, Middle Aged, Obesity, Veins
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.
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