234 Gastrokine-2 Knockout Mice Display Spontaneous Fundic Atrophy and Hypertrophy With Accelerated Progression Following Helicobacter pylori Infection

control) was added instead on the other day.Blood glucose, serum insulin, and plasma glucagon were measured from before until 240 min after ingestion of the test meal.Plasma levels of two incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), were measured until 120 min after the meal.Gastric emptying was assessed over 240 min with a 13C acetate breath test (Breath ID System, Exalenz Bioscience Ltd., Israel).Postprandial dyspeptic symptoms were assessed on a visual analogue scale.Results: The insulin peak occurred significantly earlier with MSG.Postprandial glucose was reduced by MSG, and the decrease was significant at 30 min (58.8 ± 4.4 mg/dl with MSG vs. 68.2± 4.3 mg/dl with NaCl, p=0.045 at 30 min postprandially; 53.6 ± 6.1 mg/dl vs. 66.4 ± 6.8 mg/dl, P=0.080 at 45 min).The glucagon level recovered to baseline by 120 min after the meal containing MSG.In contrast, it was still suppressed at 120 min after the meal containing NaCl.However, the area under the concentration versus time curve from 0 to 240 min (AUC (0-240)) for glucose, insulin, or glucagon was not altered by MSG.Plasma GLP-1 was significantly higher at 30 min after the meal containing MSG (58.1 ± 15.8 pmol/L with MSG vs. 13.4 ± 15.8 pmol/L with NaCl, p=0.035).Plasma GLP-1 reached its peak rapidly at 30 min postprandially with MSG, whereas it increased gradually after the meal with NaCl.The half gastric emptying time was not altered by MSG and dyspeptic symptoms were not affected by MSG.Conclusion: MSG induces a more rapid insulin response with improvement of postprandial glycemia and faster recovery of glucagon after intake of a lipid-containing liquid meal.These effects were not associated with a change of gastric emptying, but possibly with increased GLP-1 secretion.