Abstract no. 269: Intestinal Glucose Transporter (SGLT1) Expression in the Small Intestine of Control and Diabetic Rats Rasha Al-Shali University of Liverpool The ingested carbohydrates in the diet are metabolised into the simplest form of sugars by intestinal digestive enzymes, namely sucrase, maltase and lactase. Then, the dietary glucose (and galactose) is transported from the intestinal lumen to the blood stream through the small intestinal (SI) absorptive enterocytes. Glucose is transported actively by the Sodium-dependent glucose co-transport 1 (SGLT1) across the brush-border membrane (BBM), and passively by the monosaccharide transporter, GLUT2, across the basolateral membrane (BLM) of the enterocytes. The fluctuating level of luminal glucose is sensed by a glucose sensor initiating pathways to regulate the expression of SGLT1. In diabetes mellitus (DM), intestinal SGLT1 expression is enhanced leading to higher capacity of intestinal glucose absorption. This upregulated expression is independent of dietary carbohydrate intake, blood glucose concentration and insulin. This study aimed to investigate the mechanism(s) underlying the enhanced SGLT1 expression in the diabetic intestine. Control rats and experimentally streptozotocin-induced diabetic rats were used as a model of type 1 DM.The immunohistochemical staining showed that SGLT1 is expressed in more enterocytes of diabetic rats than the control in the mid and distal SI along the crypt/villus axis. Transport studies revealed that glucose uptake rates in the proximal, mid and distal small intestine are significantly increased by 10-, 5- and 5- folds, respectively, in diabetic compared to control rats. While, the mRNA levels of SGLT1 were elevated by 2, 3 and 3.7 folds, respectively, in diabetic compared to control rats. The specific activities of maltase, sucrase and alkaline phosphatase enzymes were determined and found to be generally 2.3, 3.3 and 3.5 folds higher in the intestine of diabetic compared to the control rats. The data suggest that the enhancement of SGLT1 expression and glucose uptake in the intestine of diabetic rats may be due to several causes: diabetic-induced mucosal hypertrophy, hence, more enterocytes supporting more SGLT1 along each villus, and higher expression of SGLT1 transporters per each Enterocyte.
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