Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus.

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Abstract
BACKGROUND: Hyperglycaemia delays gastric emptying, both in healthy controls and in patients with diabetes mellitus. The effect of hyperglycaemia on antroduodenal motility in diabetes has not yet been studied. AIM: To investigate the gastrointestinal motor mechanisms involved in the hyperglycaemia induced retardation of gastric emptying in patients with type I diabetes mellitus and autonomic neuropathy. In eight diabetic patients antroduodenal manometry was performed simultaneously with scintigraphic measurement of emptying of a mixed solid-liquid meal, during euglycaemia (5-8 mmol/l glucose) and hyperglycaemia (16-19 mmol/l glucose), on separate days, in random order. RESULTS: Hyperglycaemia decreased 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 antral pressure waves propagated over > or = 4.5 cm (p = 0.04). Duodenal phase III-like activity was seen irrespective of the glycaemic state (in three patients during euglycaemia and in four patients during hyperglycaemia). Hyperglycaemia significantly affected gastric emptying of the solid meal: it prolonged the lag phase from 20.0 minutes 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 of 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 during hyperglycaemia (r = 0.28, P = 0.31). Liquid emptying was not influenced by the blood glucose concentration. CONCLUSIONS: Hyperglycaemia reduces postprandial antral contractile activity and its organisation in patients 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.