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Updated: May 4, 2026

Roux-en-Y Gastric Bypass Operation in Rats
Published on: June 11, 2012
Relevance of beta-cell function for improved glycemic control after gastric bypass surgery
Jesús Blanco1, Amanda Jiménez1, Roser Casamitjana2
1Obesity Unit, Hospital Clinic Universitari, Barcelona, Spain.
Background:
Residual beta-cell function and gastrointestinal hormones have been suggested as relevant determinants of improved glycemic control ensuing Roux-en-Y gastric bypass (RYGB). The objective of this study was to compare the glycemic control up to 24 months after RYGB in C-peptide negative morbidly obese (MO) type 1 diabetes mellitus (T1 DM) women (n = 7) and C-peptide positive (>.6 ng/mL) MO women with type 2 diabetes mellitus (T2 DM, n = 7) on basal-bolus insulin therapy. The glucagon-like peptide 1 (GLP-1) and glucagon response to a mixed meal challenge were also compared between groups.
Methods:
Percent excess weight loss (%EWL), HbA1c, and daily insulin dose (DID) after RYGB were compared between groups. The GLP-1 and glucagon response (area under the curve 0-120 minutes) after a mixed meal at last follow-up visit were also compared.
Results:
At 24-months, marked %EWL was observed in women with T1 DM and women with T2 DM (mean±standard error, 82.6% ± 11.3% and 87.4% ± 30.5%, respectively; P = .722]. In women with T1 DM, HbA1c (4 months, P<.05) and DID improved transiently (P<.05, up to 8 months) but were comparable to baseline thereafter (HbA1c: baseline, 8.3 ± 1.2 and 24 months, 8.2 ± .9, P = 1.00; DID: baseline, .61 ± .17 and 24 months .62 ± .12 IU/kg/d, P = 1.00]. In contrast, in MO women with T2 DM, HbA1c decreased significantly throughout follow-up, with 2 patients presenting diabetes remission and all but one an HbA1c<7% at 24 months. The GLP-1 response was comparable between groups (P = .612), and was not accompanied by suppression of the glucagon response to meal intake.
Conclusions:
In the absence of residual beta-cell, RYGB results in no significant benefit on glycemic control, despite a marked response of GLP-1 to meal intake.
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