Atrophy of the small intestinal mucosa is functionally characterized by a reduction in non-electrolyte transport in vivo. In order to elucidate the cellular defect being responsible for this malabsorption, we have studied the Na+-dependent D-glucose accumulation as well as the activities of aminopeptidase M and maltase in brush border membrane vesicles prepared from jejunal self-emptying blind loops and corresponding intestinal segments of sham-operated control rats. Membrane vesicles from atrophic mucosa did not show any differences in D-glucose uptake or in enzyme activities when compared with those derived from normal intestine. Thus it is unlikely that the impaired non-electrolyte absorption in the atrophic mucosa in vivo is due to a defect in cellular transport processes. It is more probable that the functional impairment is the result of the diminished absorptive surface in this pathophysiological condition.