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Separate Impact of Obesity and Glucose Tolerance on the Incretin Effect in Normal Subjects and Type 2 Diabetic Patients
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OBJECTIVE—To quantitate the separate impact of obesity and hyperlycemia on the incretin effect (i.e., the gain in β-cell function after oral glucose versus intravenous glucose). RESEARCH DESIGN AND METHODS—Isoglycemic oral (75 g) and intravenous glucose administration was performed in 51 subjects (24 with normal glucose tolerance [NGT], 17 with impaired glucose tolerance [IGT], and 10 with type 2 diabetes) with a wide range of BMI (20–61 kg/m2). C-peptide deconvolution was used to reconstruct insulin secretion rates, and β-cell glucose sensitivity (slope of the insulin secretion/glucose concentration dose-response curve) was determined by mathematical modeling. The incretin effect was defined as the oral-to-intravenous ratio of responses. In 8 subjects with NGT and 10 with diabetes, oral glucose appearance was measured by the double-tracer technique. RESULTS—The incretin effect on total insulin secretion and β-cell glucose sensitivity and the GLP-1 response to oral glucose were significantly reduced in diabetes compared with NGT or IGT (P ≤ 0.05). The results were similar when subjects were stratified by BMI tertile (P ≤ 0.05). In the whole dataset, each manifestation of the incretin effect was inversely related to both glucose tolerance (2-h plasma glucose levels) and BMI (partial r = 0.27–0.59, P ≤ 0.05) in an independent, additive manner. Oral glucose appearance did not differ between diabetes and NGT and was positively related to the GLP-1 response (r = 0.53, P < 0.01). Glucagon suppression during the oral glucose tolerance test was blunted in diabetic patients. CONCLUSIONS—Potentiation of insulin secretion, glucose sensing, glucagon-like peptide-1 release, and glucagon suppression are physiological manifestations of the incretin effect. Glucose tolerance and obesity impair the incretin effect independently of one another.
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“Also, we only tested young and healthy adults and did not confirm our results in obese subjects or patients with impaired glucose metabolism (18, 37).”
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Metadata
- Authors
- Muscelli, E., Mari, A., Casolaro, A., Camastra, S., Seghieri, G., Gastaldelli, A., Holst, J. J., & Ferrannini, E.
- Affiliations
- University of Pisa (IT)
- National Research Council (IT)
- Division of Internal Medicine, Spedali Riuniti, Pistoia, Italy
- University of Copenhagen (DK)
- Corresponding author
- Ferrannini, Ele
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2008-05-01
- Volume
- 57
- Issue
- 5
- Pages
- 1340-1348
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2145818242
- Cited by
- 409
- References
- 50
- Citations by year
- 2026: 9 · 2025: 4 · 2024: 17 · 2023: 19 · 2022: 23 · 2021: 21 · 2020: 17 · 2019: 22 · 2018: 20 · 2017: 27 · 2016: 22 · 2015: 35 · 2014: 35 · 2013: 34 · 2012: 20
- FWCI
- 18.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- 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, Cardiovascular Risks, and Lipoproteins
- Keywords
- incretin effect, obesity, glucose tolerance, type 2 diabetes, impaired glucose tolerance, beta-cell function, beta-cell glucose sensitivity, glucagon-like peptide-1, glucagon suppression, insulin secretion, body mass index, hyperglycemia
- MeSH terms
- Insulin Secretion, Adult, Blood Glucose, Diabetes Mellitus, Type 2, Female, Glucose Tolerance Test, Humans, Hypoglycemic Agents, Insulin, Male, Middle Aged, Obesity, Reference Values, Body Mass Index, Insulin-Secreting Cells
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