Journal
BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
Volume 17, Issue 6, Pages 943-956Publisher
ELSEVIER SCI LTD
DOI: 10.1016/S1521-6918(03)00107-0
Keywords
glucose transport; glucose-galactose malabsorption; Fanconi-Bickel syndrome
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK044602, R01DK019567] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK44602, DK19567] Funding Source: Medline
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Carbohydrates are mostly digested to glucose, fructose and galactose before absorption by the small intestine. Absorption across the brush border and basolateral membranes of enterocytes is mediated by sodium-dependent and -independent membrane proteins. Glucose and galactose transport across the brush border occurs by a Na+/glucose (galactose) co-transporter (SGLT1), whereas passive fructose transport is mediated by a uniporter (GLUT5). The passive exit of all three sugars out of the cell across the basolateral membrane occurs through two uniporters (GLUT2 and GLUT5). Mutations in SGLT1 cause a major defect in glucose and galactose absorption (glucose-galactose Malabsorption), but mutations in GLUT2 do not appear to disrupt glucose and galactose absorption. Studies on GLUT1 null mice and Fanconi-Bickel patients suggest that there is another exit pathway for glucose and galactose that may involve exocytosis. There are no known defects of fructose absorption.
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