Introduction: Glucagon-like peptide 1 (GLP-1) reduces postprandial glycaemia by modulating gastric emptying and endocrine pancreatic secretion. Rapidly after its secretion, intact GLP-1 (7-36)amide is proteolytically cleaved by the enzyme dipeptidyl-peptidase IV, yielding the metabolite GLP-1 (9-36)amide. The effects of GLP-1 (9-36)amide on gastric emptying and insulin secretion in humans are less well characterised. Patients and methods: 14 healthy male volunteers (age: 24.2 ± 2.0 years, BMI: 24.7 ± 2.2 kg/m²) were studied with the intravenous infusion of GLP-1 (7-36)amide (1.2 pmol^. kg^-1. min^-1), GLP-1 (9-36)amide (1.2 pmol^.kg^-1. min^-1) or placebo, each administered on separate occasions over 390 min in the fasting state. After 30 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 at 30 min intervals for the determination of GLP-1 (total and intact), glucose, insulin, C-peptide and glucagon. Results: During the administration of GLP-1 (7-36)amide and GLP-1 (9-36)amide, total GLP-1 plasma levels of 139 ± 15 pmol/l and 88 ± 9 pmol/l were reached, respectively (p < 0.001 vs. placebo). Plasma concentrations of intact GLP-1 were raised to 21 ± 5 pmol/l by the infusion of GLP-1 (7-36)amide, but remained unchanged during GLP-1 (9-36)amide infusion (5 ± 3 pmol/l; p < 0.001 vs. GLP-1 (7-36)amide administration). GLP-1 (7-36)amide administration reduced fasting as well as postprandial glucose concentrations (p < 0.001) and markedly delayed gastric emptying (p < 0.001). The GLP-1 metabolite had no influence on insulin or C-peptide concentrations under fasting conditions or after the meal. Glucagon levels were lowered by GLP-1 (7-36)amide (p < 0.05), but not by GLP-1 (9-36)amide. However, the postprandial rise in glycaemia was significantly reduced (by ~6 mg/dl) by GLP-1 (9-36)amide administration (p < 0.05). In contrast, gastric emptying was completely unaffected by the GLP-1 metabolite. Conclusions: The major GLP-1 metabolite lowers postprandial glycemia independently of changes in insulin and glucagon secretion or in the rate of gastric emptying in healthy human subjects. Most likely this is due to direct effects on glucose disposal. However, the glucose-lowering potential of GLP-1 (9-36)amide appears to be small compared to that of intact GLP-1 (7-36)amide.