Colonic fermentation of organic matter to short-chain fatty acids has been implicated in the improvement in insulin sensitivity achieved by feeding diets rich in complex carbohydrates. The present study assessed the potential role of the colon in determining postprandial glucose kinetics. Metabolic responses to a complex-carbohydrate test meal were determined in conjunction with a primed continuous infusion of D-[6,6-2H]glucose in a group of ileostomists and sex-matched controls. Glucose disposal (GD) was computed using Steele's (1959) non-steady-state kinetics on a single compartment model. Insulin sensitivity was derived using cumulative GD as the dependent variable, and time and the integrated insulin concentration as independent variables. The ileostomist group had a significantly higher postprandial plasma insulin concentration ( P = 0.034) compared with the control group, but no difference in the plasma glucose concentration. Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0.46 v. 0.13 mg glucose/min per pmol, P = 0.015). The ileostomist group also showed a 50% lower rate of glucose oxidation in the postprandial period (p = 0.005), although the rate of non-oxidative GD was not significantly affected. The present study indicates that loss of the colon is associated with several characteristics of the insulin resistance syndrome, and favours a view that the colon has a role in the control of postprandial glucose.