The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Plasma Insulin Responses to Oral and Intravenous Glucose: Studies in Normal and Diabetic Subjects*
Open accessAbstract
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 [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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Cites
Somogyi, M. (1945) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)43098-0 · Cited by 1,788
Plasma Insulin Response to Oral and Intravenous Glucose Administration1
ELRICK, H., STIMMLER, L., HLAD, C. J., & ARAI, Y. (1964) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-24-10-1076 · Cited by 857
Seltzer, H. S., Allen, E. W., Herron, A. L., & Brennan, M. T. (1967) · Journal of Clinical Investigation · doi:10.1172/jci105534 · Cited by 819 · cited 1×
“(24) and Cerasi and Luft (25) that insulin secretion is impaired in diabetes mellitus.”
BackgroundNew Interpretation of Oral Glucose Tolerance
Mcintyre, N., Holdsworth, C. D., & Turner, D. S. (1964) · The Lancet · doi:10.1016/s0140-6736(64)90011-x · Cited by 738
Promotion of Insulin Secretion by Glucagon
Samols, E., Marri, G., & Marks, V. (1965) · The Lancet · doi:10.1016/s0140-6736(65)90761-0 · Cited by 521
Intestinal Factors in the Control of Insulin Secretion
McIntyre, N., Holdsworth, C. D., & Turner, D. S. (1965) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-25-10-1317 · Cited by 382
THE PLASMA INSULIN RESPONSE TO GLUCOSE INFUSION IN HEALTHY SUBJECTS AND IN DIABETES MELLITUS
Cerasi, E., & Luft, R. (1967) · Acta Endocrinologica · doi:10.1530/acta.0.0550278 · Cited by 371
Perley, M., & Kipnis, D. M. (1966) · Diabetes · doi:10.2337/diab.15.12.867 · Cited by 330
Self-citationYalow, R. S., & Berson, S. A. (1960) · Diabetes · doi:10.2337/diab.9.4.254 · Cited by 330
PLASMA INSULIN AND GROWTH HORMONE LEVELS IN OBESITY AND DIABETES
Yalow, R. S., Glick, S. M., Roth, J., & Berson, S. A. (1965) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1965.tb34803.x · Cited by 199
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Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis
Hales, C. N., & Barker, D. J. P. (1992) · Diabetologia · doi:10.1007/bf00400248 · Cited by 3,367
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Müller, T. D., Finan, B., Bloom, S. R., D'Alessio, D., Drucker, D. J., Flatt, P. R., Fritsche, A., Gribble, F., Grill, H. J., Habener, J. F., et al. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.09.010 · Cited by 1,868
Metadata
- 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 › Endocrinology, Diabetes and Metabolism › 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
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