INHIBITORY EFFECTS OF HYPERGLYCEMIA ON FED JEJUNAL MOTILITY - POTENTIAL ROLE OF HYPERINSULINEMIA

Background Acute hyperglycaemia is known to inhibit jejunal interdiges tive motility. This study was undertaken to establish the effects of h yperglycaemia on fed jejunal motility and small intestinal transit tim e, and to establish if the effects of hyperglycaemia are mediated in p art by hyperinsulinaemia. Methods Nine healthy male volunteers were st udied in random order using three experimental conditions: (a) euglyca emic clamp (glucose 5 mmol L-1); (b) hyperglycaemic clamp (glucose 15 mmol L-1); and (c) euglycaemic hyperinsulinaemic clamp (glucose 5 mmol L-1). Fed jejunal motility was induced by an intrajejunal perfusion o f lipid (Lipofundin medium-chained triglyceride 10%) at 1.5 mL min(-1) (1.5 kcal min(-1)) for 180 min through the most proximal port of a ma nometry catheter (eight ports spaced at 2-cm intervals) located just d istal to the ligament of Treitz. One minute after starting the lipid p erfusion, 15 g of lactulose dissolved in 20 mL of tap water was infuse d. Small intestinal transit time was measured by the hydrogen breath t est. Results Acute hyperglycaemia reduced the total number of jejunal contractions and progradely propagated contractions, the motility inde x (P < 0.05) and the mean amplitude of contractions and delayed intest inal transit time. Hyperinsulinaemia reduced the total number of jejun al contractions, motility index (P < 0.05) and intestinal transit time . Conclusions Thus, hyperinsulinaemia may contribute to the inhibitory effects of hyperglycaemia on jejeunal motility. In addition, this stu dy demonstrated that intrajejunal infusion of lipid stimulates sustain ed glucagon-like peptide-1 release. In contrast to fat-induced gastric inhibitory polypeptide release, this glucagon-like peptide-1 release is not inhibited by exogenous or endogenous hyperinsulinaemia (P = 0.5 9).