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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The incretin effect is increased in gastric bypass patients with type 2 diabetes.
“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]
Glucagon secretion after gastric bypass is elevated after meal ingestion.
“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]
Gastric bypass subjects have elevated plasma concentrations of GLP-1.
“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]
The relatively higher postprandial insulin responses seen in patients after gastric bypass are not a response to insulin resistance or the result of general hypersensitivity of β-cells to glucose.
“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]
The obesity-independent hypoglycemic effect of bariatric procedures has been related to the action of GLP-1 in promoting insulin secretion.
“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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“Both RYGB and VSG were shown to increase glucose-mediated GLP-1 secretion and to expedite gastric emptying time after surgery, which are thought to play key roles in increasing the risk of postbariatric surgery hypoglycemia (24,25).”
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- 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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