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

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Abstract
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.

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