Abstract

It is well known that small quantities of intact dietary sucrose and lactose pass across the normal intestinal wall, probably by a process of non-mediated diffusion, and are subsequently excreted in the urine (Folin & Berglund, 1922; Utter, 1927). Except for lactosuria during pregnancy and lactation (Brock & Hubbard, 1935) and very rare instances of endogenous sucrosuria (Elmer et al., 1939), disaccharides appearing in the urine are usually of dietary origin. Excretion of sucrose and lactose in larger amounts, associated with gastroenteritis, coeliac disease, hiatus hernia and other intestinal abnormalities, have been attributed to either disaccharidase deficiency producing elevated intestinal concentrations, or increased permeability of a structurally damaged mucosa (Moncrieff & Wilkinson, 1954; Owen L Santini et al., 1957; Bickel, 1961 ; Gryboski et al., 1963; Weser & Sleisenger, 1965). Further analysis of the factors that determine absorption of intact oligosaccharide is presented, and the clinical siginficance of increased absorption is discussed. Urinary sugar measurements presented were made by quantitative paper chromatography (Menzies, 1973).

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