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Role of Reduced Suppression of Glucose Production and Diminished Early Insulin Release in Impaired Glucose Tolerance
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BACKGROUND: Insulin resistance and impaired insulin secretion both occur in non-insulin-dependent diabetes (NIDDM), but their relative importance is unclear. Hyperglycemia itself has adverse effects on tissue insulin sensitivity and insulin secretion that make it difficult to distinguish between primary and secondary abnormalities. To avoid this problem we studied subjects with postprandial glucose intolerance but not sustained hyperglycemia. METHODS: We compared the rate of systemic appearance and disappearance of glucose, the output of endogenous hepatic glucose, splanchnic and muscle uptake of glucose, and plasma insulin and glucagon responses after the ingestion of 1 g of glucose per kilogram of body weight in 15 subjects with impaired glucose tolerance (8 of them nonobese and 7 obese) and in 16 normal subjects (9 nonobese and 7 obese) who were matched for age and weight. RESULTS: After glucose ingestion the mean (+/- SE) rate of total systemic appearance of glucose was significantly higher in both the nonobese subjects (455 +/- 12 mmol per five hours) and the obese subjects (486 +/- 17 mmol per five hours) with impaired glucose tolerance than in the respective normal subjects (411 +/- 11 and 436 +/- 7 mmol per five hours). This difference was fully accounted for by the reduced suppression of endogenous hepatic glucose in the subjects with impaired glucose tolerance (a reduction of about 28 percent, vs. 48 percent in the normal subjects; P less than 0.01). Despite late hyperinsulinemia, at 30 minutes the subjects with impaired glucose tolerance had smaller increases in plasma insulin and smaller reductions in plasma glucagon (both P less than 0.01). Molar ratios of plasma insulin to plasma glucagon levels correlated inversely (r = -0.62, P less than 0.001) with the rates of systemic glucose appearance; the latter correlated positively (r = 0.72, P less than 0.0001) with peak plasma glucose concentrations. CONCLUSIONS: Impaired glucose tolerance, the precursor of NIDDM, results primarily from reduced suppression of hepatic glucose output due to abnormal pancreatic islet-cell function. The late hyperinsulinemia may be the consequence of an inadequate early beta-cell response rather than of insulin resistance.
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“As indicated by several studies, insulin resistance leads to basal-fasting hyperinsulinemia, which may result in the insensitivity of beta-cell secretion. This insensitivity leads to a lower first-phase insulin secretion to the rising postprandial glucose but a subsequent exaggerated compensatory second-phase insulin secretion, which might result in hypoglycemia [2, 3].”
From Associated Factors with Biochemical Hypoglycemia during an Oral Glucose Tolerance Test in a Chinese Population (2017) · cites this paper as [3]
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“When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal, which leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs.[3]”
From Postprandial Reactive Hypoglycemia (2019) · cites this paper as [3]
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“Indeed, with better matching of subjects for age, sex and obesity, there also does seem to be a decrease of the insulinogenic index in subjects with IGT [5, 87, 88].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [5]
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“This reduction in the early insulin response results in a lack of adequate suppression of hepatic glucose production with subsequent post challenge hyperglycaemia and increased insulin concentrations late in the test [5, 126].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [5]
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Self-citation
Metadata
- Authors
- Mitrakou, A., Kelley, D., Mokan, M., Veneman, T., Pangburn, T., Reilly, J., & Gerich, J.
- Affiliations
- University of Pittsburgh (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1992-01-02
- Volume
- 326
- Issue
- 1
- Pages
- 22-29
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2330273698
- Cited by
- 595
- References
- 47
- Citations by year
- 2026: 12 · 2025: 5 · 2024: 9 · 2023: 11 · 2022: 15 · 2021: 15 · 2020: 13 · 2019: 13 · 2018: 14 · 2017: 20 · 2016: 12 · 2015: 27 · 2014: 25 · 2013: 18 · 2012: 19
- FWCI
- 21.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r37dk020411-19)
- National Institute of Diabetes and Digestive and Kidney Diseases (5R37 DK20411)
- National Center for Research Resources (M01RR000056, 5 M01 RR00056)
- 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 Treatment and Management
- Keywords
- impaired glucose tolerance, type 2 diabetes, hepatic glucose production, insulin secretion, hyperinsulinemia, glucagon, insulin/glucagon ratio, muscle glucose uptake, obesity, beta-cell dysfunction, insulin resistance
- MeSH terms
- Insulin Secretion, Blood Glucose, Diabetes Mellitus, Type 2, Female, Glucagon, Glucose Tolerance Test, Humans, Insulin, Islets of Langerhans, Liver, Male, Middle Aged, Muscles, Prediabetic State
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