Small intestinal transport of 3-O-methyl-D-glucose were studied in everted sacs and by circulating in situ segments in normal and diabetic rats. In circulation studies absorption was determined from net H2O movement and loss of intra-luminal 3-O-MG. In sac studies net H2O movement and 3-O-MG concentration in serosal fluid (S), mocosal fluid (M), and tissue H2O (T) were measured. The initial 3-O-MG concentration was 1 m[image] in S and M, and after 1 hr. of incubation S/M was 2.2 in normal and 4.5 in diabetic rats. T/M was 2.7 in normal and 5.9 in diabetic rats. Net 3-O-MG movement was 3 times greater in diabetic than in normal rats and followed the increase in S/M and T/Mgradients. Since T/S was 1.2 in normal and 1.3 in diabetic rats, the increased transintestinal movement of 3-O-MG in sacs from diabetic rats could be explained by increased tissue uptake. In an attempt to explain the increased uptake, the following observations were made: addition of insulin did not change significantly 3-O-MG transport in sacs from diabetic rats, addition of glucose to S of glucose to S of sacs from normal rats increased transport slightly, but significantly; addition of glucose to S and M of sacs from normal rats caused net movement of 3-O-MG from S to M; 3-O-MG absorption from in situ segments was also significantly increased in diabetic rats, but only by 20%. Hexose transport in diabetic rats does not depend directly on glucose metabolism, and cannot be explained by an increased intestinal glucose pool. Because of defective glucose metabolism the energy for increased hexose transport in diabetes must arise from other metabolic pathways.