Endocrine Abstracts (2011) 26 P735

Insulin restores salivary secretion in diabetic rats: involvement of Na+/glucose cotransporter SGLT1

R Sabino-Silva, R S Campello, H K Nakamura, H S Freitas, M M Okamoto, R C Mori & U F Machado

Department of Physiology and Biophysics, Sao Paulo, SP, Brazil.

Introduction: Considering the high capacity of water transport of Na+/glucose cotransporter SGLT1, the aim of this study was to investigate the potential role the SGLT1 in luminal membrane of ductal cells of salivary glands upon the non-stimulated salivary secretion of diabetic rats. The present study also investigates the presence of glucose transporter GLUT1 in salivary glands of rats.

Methods: Non-stimulated salivary secretion and SGLT1/GLUT1 protein (western blotting and immunohistochemistry) in parotid and submandibular glands were analyzed in non-diabetic and non-treated or insulin-treated (3, 6 and 9 U/day) diabetic Wistar rats.

Results: Diabetes increased SGLT1 protein in luminal membrane of ductal cells, which was accompanied by ~80% reduction (P<0.001) in salivary flow. Insulin treatment (6 and 9 U) decreased the SGLT1 protein expression in ductal cells of glands of diabetic rats, as compared to non-treated diabetic rats. These treatments were also able to revert (P<0.05 and P<0.01 respectively for 6 and 9 U) the diabetes-induced decrease in salivary secretion. Moreover, GLUT1 staining was observed mainly in basolateral membrane of ductal cells of salivary glands of non-diabetic and diabetic rats.

Conclusions: We propose that in the salivary glands the GLUT1 participate of reabsorption of glucose in basolateral membrane, together with the SGLT1 in luminal membrane. In diabetes, reduced salivary flow was associated with increased SGLT1 protein in luminal membrane of ductal cells of salivary glands. Furthermore, insulin treatment reduced SGLT1 in luminal membrane of ductal cells, and increased salivary flow. These SGLT1 regulations, by modulating water reabsorption, might explain the alterations of salivary secretion observed in insulin-treated or untreated diabetic rats.

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