Inhibitory effect of Shiga toxin on the expression of Na +- d-glucose cotransporter in rabbit ileum

• Published in: Nutrition research (New York, N.Y.) Vol. 26; no. 7; pp. 356 - 361
• Main Authors: Chopra, Puja, Verma, Dinesh, Khullar, Madhu, Mahmood, Safrun
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.07.2006; Elsevier Science
• Subjects: animal disease models; Biological and medical sciences; dysentery; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; gene expression; glucose transporters; ileum; intestinal absorption; malabsorption; messenger RNA; mRNA; nutrition-genotype interaction; protein synthesis; Rabbit ileum; rabbits; Shiga toxin; Shigella dysenteriae 1; shigellosis; sodium; sodium-dependent glucose transporter (SGLT1); Sodium-dependent glucose transporter (SGLT1) protein expression; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Shigella dysenteriae 1; mRNA; Shiga toxin; Sodium-dependent glucose transporter (SGLT1) protein expression; Rabbit ileum; Digestive system; Rabbit; Coupled transport; Glucose; Lagomorpha; Gene expression; Small intestine; Ileum; Toxin; Vertebrata; Mammalia; Messenger RNA; Sodium; Animal; Carrier protein
• ISSN: 0271-5317; 1879-0739
• DOI: 10.1016/j.nutres.2006.06.006

Infection by Shigella dysenteriae 1 is one of the leading causes of intestinal dysfunction; however, the underlying mechanism of this effect is largely unknown. Shigella dysenteriae 1 produces Shiga toxin, which activates Ca 2+-dependent signal transduction pathway that impairs intestinal epithelial transport. Hence, the aim of this study was to explore how the Shiga toxin affects Na +-dependent d-glucose transport in the intestine. Rabbit was used as an experimental model for these studies. Purified Shiga toxin significantly inhibited the absorption of Na +-dependent d-glucose uptake by reducing transport capacity ( V max) without affecting affinity constant ( K t) of sodium-dependent glucose transporter (SGLT1) protein in rabbit ileum. In contrast, there was no effect of the toxin on Na +-independent sugar uptake in the rabbit ileum. Western blot analysis revealed a decrease in SGLT1 protein in toxin-treated ileal loops as compared with control, but Northern blot analysis revealed no change in the mRNA levels encoding the SGLT1 protein. The present findings suggest that intestinal glucose malabsorption in Shigella infection is not related to mRNA expression encoding SGLT1, but the observed inhibition is presumably a consequence of SGLT1 protein expression.