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GLUCOSE‐GALACTOSE MALABSORPTION A Study with Biopsy of the Small Intestinal Mucosa
Author(s) -
Meeuwisse G. W.,
Dahlqvist A.
Publication year - 1968
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1968.tb07291.x
Subject(s) - malabsorption , intestinal mucosa , disaccharidase , medicine , carbohydrate metabolism , galactose , endocrinology , sodium , biochemistry , small intestine , chemistry , organic chemistry
Summary Intestinal biopsies from two patients with glucose‐galactose malabsorption have been subjected to biochemical and histological studies and the absorption of glucose, mannitol and sodium has been studied with a perfusion technique in one of the patients. No accumulation of glucose against a concentration gradient was found during in vitro incubation of mucosa from the patients. Phloridzin did not further decrease the slow glucose uptake by the mucosa. L‐Alanine uptake was normal. Intestinal mucosa from both parents of a patient with glucose‐galactose malabsorption accumulated glucose. In mucosa from patients with glucose‐galactose malabsorption disaccharidase activities were normal, sodium activation of invertase could be demonstrated and ouabain‐inhibited (pump‐) ATP‐ase activity was present. The histology was essentially normal both by light microscopy and electron microscopy. The per fusion study in vivo demonstrated not only a very slow absorption of glucose but also leakage of glucose into the lumen. Sodium absorption was not impaired. From the data obtained it is suggested that this inborn error of metabolism is localized at the level of the glucose‐galactose membrane carrier of the small intestinal mucosa.