Objective. The incretin hormones, GIP and GLP-1, augment post-prandial glucose-mediated insulin release from pancreatic -cells. The Goto-Kakizaki (GK) rat is a widely-used, lean rodent model of type 2 diabetes; however, little is known regarding the incretin secretion profile to different nutrients in these rats. We have recently shown that lymph is a sensitive medium to measure incretin secretion in rodents and probably the preferred compartment for GLP-1 monitoring. To characterize the meal-induced incretin profile, we compared lymphatic incretin concentrations in the GK and Wistar rat after enteral macronutrient administration. Methodology. After cannulation of the major mesenteric lymphatic duct and duodenum, each animal received an intra-duodenal bolus of either a fat emulsion, dextrin, a mixed meal, or saline. Lymph was collected for 3 hours and analyzed for triglyceride, glucose, GLP-1 and GIP content. Results. There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. Dextrin and a mixed meal both increased incretin concentration AUC, however significantly less in GK rats compared to Wistar rats (dextrin GIP: 707 (pg/ml)hr ± 106 versus 1373 (pg/ml)hr ± 114 respectively, p<0.001; dextrin GLP-1: 82.7 (pM)hr ± 24.3 versus 208.3 (pM)hr ± 26.3 respectively, p=0.001). Conclusions. After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared to Wistar rats, a phenomenon not seen after a lipid meal. We propose a similar, glucose-mediated incretin secretion pathway defect of both K and L cells in GK rats.