Background. Approximately 20% of patients with FD have rapid gastric emptying (RGE). Accelerated duodenal delivery of nutrients and/or increased duodenal sensitivity may explain GI symptoms in these patients. Indeed, FD patients report severe symptoms during duodenal lipid (LIP)) but not carbohydrate (CHO) infusion. The mechanisms of this increased sensitivity are poorly understood. While enteral hormones are implicated, there is limited evidence, only for CCK, based on a study of 8 functional dyspepsia patients and 8 controls (Pilichiewicz 2008). Hypotheses. Patients with FD have increased nutrient sensitivity and concentrations of plasma enteral hormones mediating satiety during duodenal enteral lipid or CHO infusion. Methods. Enteral hormonal responses during duodenal nutrient infusion were compared in 35 healthy subjects (41 ± 3 years, 24 females, BMI 26.4 ± 0.7 kg/m2) and 30 FD patients (40 ± 3 years, 26 female, BMI 26.4 ± 0.7 kg/m2) with previously documented idiopathic RGE for solids. Isocaloric (222 kcal) and isovolumic (222 mL) carbohydrate (CHO, Limeondex®, 75 gm) and lipid infusions (Microlipid® 66.7 mL diluted to 222 mL, 0.5 gm/mL) were administered in randomized order over 120 minutes separated by a 120minute washout period. These nutrients were given at a variable rate, approximating that at which oral glucose enters the systemic circulation in healthy subjects. During infusions, symptoms were evaluated by a VAS scale (0=none, 1=light, 2=moderate, 3=severe, 4=intolerable). Associations between plasma hormones (AUC) and subject status (ie, control vs functional dyspepsia) and separately with any moderate symptoms or worse were evaluated by univariate tests. Results. 30 controls and 24 pts completed studies. During lipid (6 controls, 14 pts) and carbohydrate infusion (1 control, 14 pts) the presence of one or more symptoms of at least moderate severity was more common (p ≤ 0.01) in patients than controls. Compared to subjects with mild or no symptoms, a higher proportion of subjects with moderate or more severe symptoms had abnormal (ie, >90th %tile values in controls) plasma hormone concentrations during the corresponding nutrient infusion ie (a) higher GLP-1 (p = 0.005) concentration during CHO infusion and (b) higher GIP (p = 0.01) and CCK (p=0.03) concentration during lipid infusion. Other hormones (PYY, ghrelin, glucagon, and insulin) were not associated with increased sensitivity. Conclusions. During enteral carbohydrate or lipid infusions, patients with FD and RGE have increased symptoms which is associated with higher plasma concentrations of GLP-1 during carbohydrate as also CCK and GIP concentrations during lipid infusion compared to controls. These data suggest that among patients with FD, enteral hormones mediate exaggerated increased intestinal sensitivity to nutrients in a nutrient-specific manner. Comparison of Plasma Hormone Concentration in Subjects with and without Moderate/ Severe/Intolerable Symptoms during Carbohydrate or Lipd Infusion