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Research article summary (published 20 Apr 2008):

Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with type 2 diabetes.

Full Abstract

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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Author information

Author/s: Laferrère, Blandine (B); Teixeira, Julio (J); McGinty, James (J); Tran, Hao (H); Egger, Joseph R (JR); Colarusso, Antonia (A); Kovack, Betty (B); Bawa, Baani (B); Koshy, Ninan (N); Lee, Hongchan (H); Yapp, Kimberly (K); Olivan, Blanca (B);

Affiliation: St. Lukes Roosevelt Hospital, Obesity Research Center, 1111 Amsterdam Avenue, New York, NY 10025, USA. BBL14@columbia.edu

Grants: 1UL1 RR 024156-02 (Agency:United States NCRR) ; DK 26687 (Agency:United States NIDDK) ; DK 63068-05 (Agency:United States NIDDK) ; R01 DK 67561 (Agency:United States NIDDK)

Journal and publication information

Publication Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

Journal: The Journal of clinical endocrinology and metabolism (J Clin Endocrinol Metab), published in United States. (Language: eng)

Reference: 2008-Jul; vol 93 (issue 7) : pp 2479-85

Dates: Created 2008/07/11; Completed 2008/08/21;

PMID: 18430778, status: MEDLINE (last retrieval date: 11/6/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Blood Glucose (0) ; Incretins (0) ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5)

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