GASTROINTESTINAL MOTOR MECHANISMS IN HYPERGLYCEMIA-INDUCED DELAYED GASTRIC-EMPTYING IN TYPE-I DIABETES-MELLITUS

Background-Hyperglycaemia delays gastric emptying, both in healthy con trols and in patients with diabetes mellitus. The effect of hyperglyca emia on antroduodenal motility in diabetes has not yet been studied. A im-To investigate the gastrointestinal motor mechanisms involved in th e hyperglycaemia induced retardation of gastric emptying in patients w ith type I diabetes mellitus and autonomic neuropathy. In eight diabet ic patients antroduodenal manometry was performed simultaneously with scintigraphic measurement of emptying of a mixed solid-liquid meal, du ring euglycaemia (5-8 mmol/l glucose) and hyperglycaemia (16-19 mmol/l glucose), on separate days, in random order. Results-Hyperglycaemia d ecreased the cumulative antral motility index from 38.3 (range 24.2-47 .6) to 30.8 (range 17.3-38.1) (p=0.025) and reduced the number of antr al pressure waves propagated over greater than or equal to 4.5 cm (p=0 .04). Duodenal phase III-like activity was seen irrespective of the gl ycaemic state (in three patients during euglycaemia and in four patien ts during hyperglycaemia). Hyperglycaemia significantly affected gastr ic emptying of the solid meal: it prolonged the lag phase fi om 20.0 m inutes to 28.5 minutes (p=0.02), increased the 50% emptying time from 73.5 minutes to 104.5 minutes (p=0.03), and increased the percentage o f isotope remaining in the stomach after 120 minutes from 33.5% to 46. 5% (p=0.02). The cumulative antral motility index was correlated with the 50% emptying time (r=0.75, p=0.02) during euglycaemia, but not dur ing hyperglycaemia (r=0.28, p=0.31). Liquid emptying was not influence d by the blood glucose concentration. Conclusions-Hyperglycaemia reduc es postprandial antral contractile activity and its organisation in pa tients with type I diabetes and autonomic neuropathy. These changes in antroduodenal motility are likely to constitute the mechanism through which gastric emptying of solids is delayed during high blood glucose concentrations in these diabetic patients.