Author/year Type of study Subjects Preop BMI % weight loss F/U time Change in hormone Morínigo et al. 2006 [51 ] Prospective controlled 9 (7 F) RYGB non diabetic 6 obese (4 F)
4
7
.
4
±
6
.
1
4
3
.
6
±
7
.
9
NA 6 wk Greater increase in active GLP-1 postmeal in RYGB group postop compared to weight-matched obese Laferrère et al. 2007 [50 ] Prospective controlled 8F T2DM RYGB 7 non diabetic obese
4
3
.
6
±
6
.
8
3
7
.
1
±
1
1
.
6
NA 1 mo Fasting- and glucose-stimulated GLP-1 similar in S and C 1 month after RYGB, increase in GLP-1 (total and active) in response to oral glucose Reinehr et al. 2007 [59 ] Prospective controlled 30 obese (26 F) 19 RYGB 11 GB
4
5
.
7
±
7
.
4
50% 2 y Decrease in fasting GLP-1 in both groups Le Roux et al. 2007 [56 ] Double-blind randomized prospective controlled 7 RYGB 6 AGB
4
4
.
5
±
2
.
9
4
1
.
9
±
7
.
5
NA
9
.
5
±
1
.
5
mo
1
7
±
1
.
4
moEarly (2 d) and increased responses of PP GLP-1 in RYGB group only Laferrère et al. 2008 [49 ] Prospective controlled 9 F T2D RYGB 10 F T2D diet induced weight loss
4
3
.
3
±
6
.
2
4
3
.
3
±
3
.
6
NA 1 mo 10 Kg weight loss Increase in total GLP-1 after oral glucose and GLP-1 AUC after RYGB but not after diet Peterli et al. 2009 [54 ] Randomized prospective controlled 13 RYGB 14 LSG
4
7
±
6
.
4
4
5
.
7
±
6
.
7
NA 1 wk and 3 mo Increased PP GLP-1 RYGB > LSG Clements et al. 2004 [61 ] Prospective uncontrolled 20 obese (15 F) with T2D
5
2
.
7
±
8
.
8
NA 2, 6, and 12 wk postop No change in fasting GLP-1 at any time point Rubino et al. 2004 [60 ] Prospective uncontrolled S: 10 (9 F, 6 T2D) obese RYGB 46.2 NA 3 wk No change in fasting GLP-1 in postop Borg et al. 2006 [57 ] Prospective uncontrolled 6 RYGB 48.3 NA 1, 3, 6 mo postop PP GLP-1 AUC increased at 6 mo postop Morínigo et al. 2006 [52 ] Prospective uncontrolled 34 RYGB (23 F, 12 NGT, 12 IGT, 10 T2D)
4
9
.
1
±
1
.
0
NGT:
3
4
.
5
±
1
.
4
IGT:
2
9
.
2
±
1
.
9
DM:
3
2
.
0
±
2
.
4
6 wk 12 mo Increase in PP GLP-1 AUC response in IGT and NGT at 6 wk Increase in PP GLP-1 AUC response in all 3 groups at 12 mo De Carvalho et al. 2009 [53 ] Prospective uncontrolled 11 NGT (9 F) RYGB 8 AGM (4 T2DM, 4 IGT) (7 F) RYGB
4
6
.
1
±
2
.
2
7
4
6
.
5
±
2
.
0
4
%
3
9
.
3
±
2
.
2
4
3
6
.
4
±
2
.
6
T1: First evaluation T2: presurgery T3: 9 mo after surgery Increase in GLP-1 levels after OGTT in both groups at T3 Kashyap et al., 2010 [73 ] Prospective uncontrolled 16 (7 F) T2D 9 RYGB 7 GR
4
7
±
9
10% 4 wk No change in fasting GLP-1 in both groups Increase in PP GLP-1 response in RYGB group only Le Roux et al. 2006 [55 ] Cross-sectional controlled 6 RYGB 6 GB 12 obese 15 lean 49.8 46.1 47.1 23.8 NA 6 to 36 mo Higher postprandial GLP-1 response in RYGB group compared to fasting levels and to other groups Korner et al. 2007 [58 ] Cross-sectional controlled 13 F non diabetic RYGB 10 F BND 13 F OW
3
1
.
3
±
1
.
3
3
6
.
1
±
1
.
7
3
6
.
1
±
2
.
2
3
5
.
6
±
2
.
4
2
4
.
6
±
2
.
3
2
4
.
6
±
2
mo postopFasting GLP-1 similar in all groups At 30 min postmeal, GLP-1 higher in RYGB group compared to BND and OW GLP-1 AUC at 180 min greater in RYBG group compared to other groups Rodieux et al. 2008 [41 ] Cross-sectional controlled 8 RYGB 6 GB 8 weight matched
4
4
.
9
±
1
.
8
4
1
.
1
±
0
.
5
2
9
.
2
±
0
.
8
4
7
.
8
±
3
.
3
3
2
.
4
±
2
.
0
9 to 48 mo (RYGB) 25 to 85 mo (GB) No difference in fasting GLP-1 between 3 groups; Exaggerated GLP-1 PP Response in RYGB.