Introduction: The insulinotropic gut hormone gastric inhibitory polypeptide (GIP) has been demonstrated to inhibit gastric acid secretion and was proposed to possess "enterogastrone" activity. GIP effects on gastric emptying have not yet been studied. Patients and methods: 15 healthy male volunteers (23.9 ± 3.3 years, BMI 23.7 ± 2.3 kg/m²) were studied with the intravenous infusion of GIP (2 pmol ^. kg^{-1 .} min^-1) or placebo, each administered on separate occasions from -30 to 360 min in the fasting state. At 0 min, a solid test meal (250 kcal; containing ¹³C-sodium-octanoate) was served. Gastric emptying was calculated from the ¹³CO₂ exhalation rates in breath samples collected over 360 min. Venous blood was drawn in 30 min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). Statistics: Repeated-measures ANOVA and one-way ANOVA. Results: During the infusion, GIP rose to steady-state concentrations of 159 ± 15 pmol/l for total and 34 ± 4 pmol/l for intact GIP (p < 0.0001). Meal ingestion further increased GIP concentrations in both groups, reaching peak levels of 265 ± 20 and 82 ± 9 pmol/l for total and 67 ± 7 and 31 ± 9 pmol/l for intact GIP during the administration of GIP and placebo, respectively (p < 0.0001). There were no differences in glucose, insulin, C-peptide between the experiments with the infusion of GIP or placebo. Gastric half emptying times were 120 ± 9 min and 120 ± 18 min (p = 1.0; with GIP and placebo, respectively). The time pattern of gastric emptying was similar in both groups (p = 0.98). Endogenous GIP secretion, as derived from the incremental AUC of plasma GIP concentrations in the placebo experiments did not correlate to gastric half emptying times (r² = 0.15, p = 0.15 for intact GIP, r² = 0.21, p = 0.086 for total GIP). Conclusions: Gastric emptying does not appear to be influenced by GIP. The secretion of GIP after meal ingestion is not suppressed by its exogenous administration. The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1.