DOSE-DEPENDENT INHIBITION OF POSTPRANDIAL GALLBLADDER MOTILITY AND PLASMA-HORMONE SECRETION DURING ACUTE HYPERGLYCEMIA

Background: Actual blood glucose concentrations influence gastrointest inal function. We investigated whether in healthy subjects the inhibit ory effect of acute hyperglycemia on gallbladder motility is dose-depe ndent. Methods: Seven healthy volunteers were studied on four separate occasions in random order during euglycemia and during hyperglycemic clamping, at 4 mmol/l, 8 mmol/l, 12 mmol/l, and 16 mmol/l, respectivel y. Gallbladder volumes (ultrasonography) and plasma hormone release we re studied before and after ingestion of a meal. Results: Postprandial gallbladder contraction was significantly (P < 0.05) and dose-depende ntly inhibited during the hyperglycemic experiments at 8, 12, and 16 m mol/l (56% +/- 8%, 49% +/- 8%, and 30% +/- 5%, respectively) compared with euglycemia (68% +/- 6%). Postprandial cholecystokinin release was significantly (P < 0.05) reduced compared with euglycemia only at a p lasma glucose level of 16 mmol/l (116 +/- 28 Versus 159 +/- 13 pmol . l(-1). 120 min). Plasma pancreatic polypeptide secretion, as an indire ct measure of vagal-cholinergic tone, was significantly (P < 0.05) and dose-dependently reduced during hyperglycemia at 8, 12, and 16 mmol/l . Conclusion: In healthy subjects acute hyperglycemia significantly an d dose-dependently inhibits postprandial gallbladder motility. Future studies on gallbladder motility should take into account the influence of plasma glucose, because already at postprandial glucose levels gal lbladder motility is reduced.