Chronic acarbose-feeding increases GLUT1 protein without changing intestinal glucose absorption function

Abstract

As α-glucosidase inhibitor, the antidiabetic drug acarbose reduces postprandial glucose levels by retarding the intestinal digestion of polysaccharides. However, it is unknown if acarbose also affects the expression of intestinal glucose transporters, especially the Na +-glucose cotransporter (SGLT1) and the glucose transporters GLUT1 and GLUT2. To unravel this question, Wistar rats received standard powdered chow either without (control) or with acarbose (40 mg acarbose/100 g chow) for 40 days. While food intake was slightly enhanced by acarbose, the drug had no influence on weight gain or plasma glucose and insulin levels. The acarbose-treatment did not alter the SGLT1 and GLUT2 gene expression in both upper and middle small intestine, whereas GLUT1 protein was increased by 75% in middle small intestine. Despite the territorial change in GLUT1 protein, the intestinal glucose absorption in an acarbose-free perfusion study was unaltered. In conclusion, the chronic use of acarbose did not alter the acarbose-free glucose absorption profile.