Ileal brake failure in streptozotocin-induced diabetic rat

Diabetes mellitus frequently alters gastrointestinal function, but the pathophysiology of the diabetic gut has not been fully elucidated. Our aim was to characterize the enterogastric modulation of gastric emptying in an experimental model of diabetic rat and to determine the putative consequences of impaired regulation on glycaemic control.

Studies were performed in streptozotozin-induced diabetic and control groups of male Sprague-Dawley rats. In rats fitted with chronic ileal cannulae, gastric emptying of a peptide meal was measured during ileal infusion of either lipids (ileal brake) or saline. The influence of the ileal brake mechanism on blood glucose levels after oral administration of a glucose solution was also evaluated.

Diabetic rats exhibited a precipitous gastric emptying (80% +/- 3% versus 57% +/- 3% in controls; P < 0.05). Ileal lipids delayed gastric emptying in control (38 +/- 4%; P < 0.05 versus ileal saline) but not in diabetic animals (77 +/- 5%; N.S. versus ileal saline). As the ileal brake contributes to the management of postprandial blood glucose levels (114 +/- 4.9 mg/dL after ileal lipids versus 134 +/- 7.8 mg/dL after ileal saline in control rats; P < 0.05), the failure of this mechanism in diabetic rats worsens glycaemic control after feeding (455 +/- 20.4 mg/dL after ileal lipids versus 399 +/- 8.7 mg/dL after ileal saline; P < 0.05).

Experimental diabetes impairs the ileal brake mechanism and disturbs gastric emptying. These abnormalities may contribute to difficult glycaemic control.