3-O-methyl-glucose is described as a good marker for glucose transport, since it is not metabolized in the enterocytes. During energy deficits, the maximal intestinal capacity for glucose absorption is of vital interest. The measured flux rates might be deviated by a metabolic degradation of (3H)-glucose, by different transporter affinities for glucose and 3-O-methyl-glucose, and by a metabolic need for glucose to achieve the full transport capacity. We therefore incubated adjacent pieces of porcine jejunum in Ussing chambers and measured short circuit current (Isc) and absorptive "glucose fluxes" on the basis of added glucose marked with (3H)-glucose or 3-O-methyl-(3H)-glucose, and added 3-O-methyl-glucose marked with 3-O-methyl-(3H)- glucose. (3H)-glucose flux rates (and Isc) increased with glucose concentration and mostly decreased after addition of phloretin and phlorizin. 3-O-methyl-(3H)-glucose resulted in 2- to 5-fold lower flux rates, independent of a putative metabolic stimulation with glucose. Phloretin only marginally decreased these flux rates, while phlorizin had no further effect. 3-O-methyl-glucose induced almost no increase in Isc. We conclude that glucose and 3-O- methyl-glucose are transported with different affinites by porcine SGLT1 (and GLUT2) and that besides these two proteins additional pathways contribute to intestinal glucose transport across porcine jejunum.