Restrictions in dietary N supply induce substantial changes in gastrointestinal protein turnover and intermediary metabolism which may lead to reductions in feed intake, growth and protein accretion. So far, there are only few experimental data on potential effects of N restriction on intestinal carbohydrate metabolism and therefore, it was the aim of the present study to characterize N effects on intestinal glucose transport. The experiments were performed in 10 goats (24.0 4.2 kg, 3 months of age). The animals were allotted to two iso-energetic feeding groups with either an adequate N supply or a reduced N supply (140 or 81 g crude protein/kg concentrate, respectively). At the end of an adaptation period of 6 to 8 weeks segments from the proximal jejunum mounted in standard Ussing chambers and incubated with a modified Krebs-Henseleit buffer solution at 38°C under continuous equilibration with carbogen. Twenty min after mounting, 185 kBq 3H-labelled 3-O-methyl-glucose (3OMG) were added to either the mucosal or serosal side of paired tissues as a tracer for measuring unidirectional glucose flux rates. Flux measurements in the absence of electrochemical gradients were performed under control conditions and after the addition of phlorizin (1 mmol/l) to the mucosal compartment. In addition, glucose-induced increases of short-circuit currents (Isc) were recorded for a rough estimate of glucose sensitivity and maximum capacity of sodium/glucose cotransport by adjusting the mucosal glucose concentrations stepwise from 0 to 15 mmol/l. N restriction resulted in significantly higher 3OMG flux rates from the mucosal to the serosal side. Since the flux rates in the opposite direction remained unaffected, N restriction induced significant increases in net flux rates which can be explained by respective stimulation of active glucose absorption. In both feeding groups, phlorizin decreased net glucose flux rates by more than 90% indicating that glucose transport was mainly mediated by sodium-coupled glucose cotransporter SGLT1. This may also be confirmed by glucose-stimulated increases in Isc in both feeding groups. At a mucosal concentration of either 1 mmol/l 3OMG or same amount of glucose maximal Isc responses were more than twice as high in tissues from N restricted animals. And this again could almost completely be blocked by phlorizin. The present data are the first evidence for effects of dietary N supply on intestinal glucose transport. Several factors such as changes in intestinal proliferation, turnover of enterocytes or compensatory intermediary responses to N restriction have to be discussed as the physiological basis for these effects.