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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/G479    most recent 00566.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Miró-Queralt, M. Articles by Planas, J. M. PubMed PubMed Citation Articles by Miró-Queralt, M. Articles by Planas, J. M.

MUCOSAL BIOLOGY

Sodium tungstate decreases sucrase and Na⁺/D-glucose cotransporter in the jejunum of diabetic rats

¹Departament de Fisiologia (Farmàcia), and Institut de Recerca en Nutrició i Seguretat Alimentària (INSA), Universitat de Barcelona; and ²Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, and Institut de Recerca Biomèdica (IRB Barcelona), Barcelona, Spain

Submitted 5 December 2007 ; accepted in final form 8 July 2008

Sodium tungstate reduces glycemia and reverts the diabetic phenotype in several induced and genetic animal models of diabetes. Oral administration of this compound has recently emerged as an effective treatment for diabetes. Here we examined the effects of 30 days of oral administration of tungstate on disaccharidase and Na⁺/D-glucose cotransporter (SGLT1) activity in the jejunum of control and streptozotocin-induced diabetic rats. Diabetes increased sucrase-specific activity in the jejunal mucosa but did not affect the activity of lactase, maltase, or trehalase. The abundance and the maximal rate of transport of SGLT1 in isolated brush-border membrane vesicles also increased. Tungstate decreased sucrase activity and normalized SGLT1 expression and activity in the jejunum of diabetic rats. Furthermore, tungstate did not change the affinity of SGLT1 for D-glucose and had no effect on the diffusional component. In control animals, tungstate had no effect on disaccharidases or SGLT1 expression. Northern blot analysis showed that the amount of specific SGLT1 mRNA was the same in the jejunum from all experimental groups, thereby indicating that changes in SGLT1 abundance are due to posttranscriptional mechanisms. We conclude that the antidiabetic effect of tungstate is partly due to normalization of the activity of sucrase and SGLT1 in the brush-border membrane of enterocytes.

diabetes mellitus; glucose transport; SGLT1; brush-border membrane vesicles