Hamster intestinal disaccharide absorption: extracellular hydrolysis precedes transport of the monosaccharide products.

Hydrolase-related transport was re-investigated in hamster small intestine by the tissue accumulation method. The Na+-dependent, phlorizin-sensitive monosaccharide transport system saturates with 30 mM-D-glucose. According to the hydrolase-related transport hypothesis, additional glucose units will be taken up if they are given in the form of a disaccharide susceptible to hydrolysis. But in experiments with [14C]sucrose we found no evidence for any such surplus glucose uptake. The uptake of 14C label from sucrose was abolished by using Tris, a strong inhibitor of sucrase, by adding competitive inhibitors of the D-glucose transport system (D-glucose, beta-methyl-D-glucopyranoside or phlorizin), and by substituting Li+ for the Na+ in the incubation medium. Glucose and fructose derived from sucrose did not enter the tissues in equimolar amounts: the glucose moiety was taken up much faster. We conclude that in hamster intestine there is no evidence for the existence of hydrolase-related transport with sucrose as the monosaccharide donor. The enzymatic hydrolysis of sucrose and the transport of its products, glucose and fructose, are two distinct events, acting sequentially.