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Effect of Weight Loss by Gastric Bypass Surgery Versus Hypocaloric Diet on Glucose and Incretin Levels in Patients with Type 2 Diabetes
Open accessAbstract
CONTEXT: Gastric bypass surgery (GBP) results in rapid weight loss, improvement of type 2 diabetes (T2DM), and increase in incretins levels. Diet-induced weight loss also improves T2DM and may increase incretin levels. OBJECTIVE: Our objective was to determine whether the magnitude of the change of the incretin levels and effect is greater after GBP compared with a low caloric diet, after equivalent weight loss. DESIGN AND METHODS: Obese women with T2DM studied before and 1 month after GBP (n = 9), or after a diet-induced equivalent weight loss (n = 10), were included in the study. Patients from both groups were matched for age, body weight, body mass index, diabetes duration and control, and amount of weight loss. SETTING: This outpatient study was conducted at the General Clinical Research Center. MAIN OUTCOME MEASURES: Glucose, insulin, proinsulin, glucagon, gastric inhibitory peptide (GIP), and glucagon-like peptide (GLP)-1 levels were measured after 50-g oral glucose. The incretin effect was measured as the difference in insulin levels in response to oral and to an isoglycemic iv glucose load. RESULTS: At baseline, none of the outcome variables (fasting and stimulated values) were different between the GBP and diet groups. Total GLP-1 levels after oral glucose markedly increased six times (peak:17 +/- 6 to 112 +/- 54 pmol/liter; P < 0.001), and the incretin effect increased five times (9.4 +/- 27.5 to 44.8 +/- 12.7%; P < 0.001) after GBP, but not after diet. Postprandial glucose levels (P = 0.001) decreased more after GBP. CONCLUSIONS: These data suggest that early after GBP, the greater GLP-1 and GIP release and improvement of incretin effect are related not to weight loss but rather to the surgical procedure. This could be responsible for better diabetes outcome after GBP.
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“Previous studies have established that the incretin effect, β-cell secretion activated by eating, is increased in GB patients with type 2 diabetes (6,9).”
From Gastric Bypass Surgery Enhances Glucagon-Like Peptide 1–Stimulated Postprandial Insulin Secretion in Humans (2011) · cites this paper as [9]
In the citing paper
“Previous studies have reported that glucagon secretion after GB is elevated after meal ingestion (9,16,25)”
From Gastric Bypass Surgery Enhances Glucagon-Like Peptide 1–Stimulated Postprandial Insulin Secretion in Humans (2011) · cites this paper as [9]
In the citing paper
“GB subjects have elevated plasma concentrations of GLP-1 (6,8–13).”
From Gastric Bypass Surgery Enhances Glucagon-Like Peptide 1–Stimulated Postprandial Insulin Secretion in Humans (2011) · cites this paper as [9]
In the citing paper
“These findings suggest that the relatively higher postprandial insulin responses seen in patients after GB (8,9,12,23) are not a response to insulin resistance or the result of general hypersensitivity of β-cells to glucose.”
From Gastric Bypass Surgery Enhances Glucagon-Like Peptide 1–Stimulated Postprandial Insulin Secretion in Humans (2011) · cites this paper as [9]
In the citing paper
“this obesity-independent hypoglycemic effect has been related to the action of GLP-1 in promoting insulin section [3], [6].”
From Treatment of obesity and diabetes using oxytocin or analogs in patients and mouse models (2013) · cites this paper as [6]
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Metadata
- Authors
- Laferrère, B., Teixeira, J., McGinty, J., Tran, H., Egger, J. R., Colarusso, A., Kovack, B., Bawa, B., Koshy, N., Lee, H., Yapp, K., & Olivan, B.
- Affiliations
- Obesity Research Center (B.L., H.T., J.R.E., A.C., B.K., B.B., K.Y., B.O.), St. Luke’s/Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York 10025
- Bariatric Division (J.T., J.M., N.K., H.L.), St. Luke’s/Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York 10025
- St. Luke's-Roosevelt Hospital Center (US)
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2008-07-01
- Volume
- 93
- Issue
- 7
- Pages
- 2479-2485
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC2453054
- OpenAlex
- W2146737709
- Cited by
- 682
- References
- 57
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 11 · 2023: 18 · 2022: 17 · 2021: 25 · 2020: 25 · 2019: 39 · 2018: 21 · 2017: 45 · 2016: 48 · 2015: 44 · 2014: 57 · 2013: 72 · 2012: 59
- FWCI
- 63.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 67561, DK63068-05, DK 26687, R01DK067561, P30DK026687)
- National Center for Research Resources (UL1RR024156)
- Topics
- Health Sciences › Medicine › Surgery › Bariatric Surgery and Outcomes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- gastric bypass, type 2 diabetes, weight loss, incretin effect, glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, proinsulin, glucagon, insulin, postprandial blood glucose, hypocaloric diet, obesity, women
- MeSH terms
- Adult, Blood Glucose, Diabetes Mellitus, Type 2, Diet, Reducing, Female, Gastric Inhibitory Polypeptide, Glucagon, Humans, Male, Middle Aged, Obesity, Gastric Bypass, Weight Loss, Glucagon-Like Peptide 1, Incretins
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