Introduction. Roux-en-y gastric bypass results in the rapid resolution of type 2 diabetes in 80-90% of morbidly obese patients. RYGB involves gastric restriction, duodenal exclusion and early hindgut stimulation by nutrients. Separating metabolic and hormonal changes due to the surgery from those due to weight loss has been difficult. We hypothesized that in diabetic Goto-Kakizaki (GK) rats early stimulation of hormone release from the hindgut accounts for improved glucose homeostasis, independent of weight loss. We compared 2 metabolic surgeries that cause early hindgut stimulation, ileal transposition (IT) and duodenal-jejunal exclusion (DJE), in GK rats. Methodology. DJE bypasses the duodenum and first 10 cm of the jejunum with a 15 cm jejunal limb. IT involves transposing a 10 cm segment of ileum into the jejunum, 10 cm distal to the ligament of Treitz. We performed a DJE, IT, DJE Sham, and IT Sham on male, 14 week old GK rats (n=9 per group), and monitored the responses for 5 wk. An oral glucose tolerance test (OGTT) was performed at 0, 2, and 4 weeks post-operatively. At 5 weeks a jugular catheter was inserted and incretin hormones were measured after a mixed meal gavage. Results. There was no difference in body weight or food intake among any of the GK groups at the end of the 30 day study period. A statistically significant improvement in the OGTT was noted at 4 weeks in DJE and IT rats (mean glucose at 120 min ± SE: DJE 198.4 ± 10.6 vs DJE Sham 241.2 ± 15.0, p=0.03; IT 191.7 ± 17.4 vs IT Sham 242.4 ± 8.2, p=0.02). Insulin concentrations during the OGTT did not differ in the DJE/IT and Sham rats, nor did the response to an insulin tolerance test. Plasma GLP-1 levels 30 min after a mixed meal were elevated in both DJE and IT rats (DJE: 4.51 ± 0.36 vs DJE Sham 2.75 ± 0.22, p=0.001; IT 4.38 ± 0.52 vs IT Sham 3.06 ± 0.25, p=0.005). Conclusions. In GK rats, DJE and IT improve glucose tolerance, suggesting that hindgut stimulation is the responsible factor. This is supported by the comparable increase in the incretin GLP-1 after both surgical procedures. Neither surgery resulted in a statistically significant increase in insulin secretion or improvement in insulin sensitivity, leading us to postulate that the primary mechanism in this model is in an extra-pancreatic action of GLP-1.