The goal of this study was to understand the mechanisms of greater weight loss by gastric bypass (GBP) compared to gastric banding (GB) surgery. Obese weight- and age-matched subjects were studied before (T0), after a 12 kg weight loss (T1) by GBP (n = 11) or GB (n = 9), and at 1 year after surgery (T2). peptide YY(3-36)(PYY(3-36)), ghrelin, glucagon-like peptide-1 (GLP-1), leptin, and amylin were measured after an oral glucose challenge. At T1, glucose-stimulated GLP-1 and PYY levels increased significantly after GBP but not GB. Ghrelin levels did not change significantly after either surgery. In spite of equivalent weight loss, leptin and amylin decreased after GBP, but not after GB. At T2, weight loss was greater after GBP than GB (P = 0.003). GLP-1, PYY, and amylin levels did not significantly change from T1 to T2; leptin levels continued to decrease after GBP, but not after GB at T2. Surprisingly, ghrelin area under the curve (AUC) increased 1 year after GBP (P = 0.03). These data show that, at equivalent weight loss, favorable GLP-1 and PYY changes occur after GBP, but not GB, and could explain the difference in weight loss at 1 year. Mechanisms other than weight loss may explain changes of leptin and amylin after GBP.

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: To determine whether the magnitude of the change of the incretin levels and effect is greater after GBP compared to 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). Patients from both groups were matched for age, body weight, BMI, diabetes duration and control, and amount of weight loss. Setting: Outpatient GCRC. Main Outcome Measures: Glucose, insulin, proinsulin, glucagon, GIP and GLP-1 levels were measured after 50 gr 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 the diet group. Total GLP-1 levels after oral glucose markedly increased 6 times (peak:17+/-6 to 112+/-54 pmol/L, p<0.001) and the incretin effect increased 5 times (9.4+/-27.5% to 44.8+/-12.7%, p<0.001) after GBP but not after diet. Post-prandial 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.