title: Chronic acarbose-feeding increases GLUT1 protein without changing intestinal glucose absorption function.
abstract: As alpha-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.
authors.affiliation: Department of Physiology and Biophysics, University of São Paulo, Av. Prof. Lineu Prestes 1524, 05508-900, São Paulo, Brazil.
authors.forename: Leonardo
authors.initials: L
authors.lastname: Paiva
authors.forename: Ralf
authors.initials: R
authors.lastname: Binsack
authors.forename: Ubiratan Fabres
authors.initials: UF
authors.lastname: Machado
mesh_terms: D020909:Acarbose / Q000008:administration & dosage*; D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D004435:Eating / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000008:administration & dosage*; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1; D051273:Glucose Transporter Type 2; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007328:Insulin / Q000097:blood; D007408:Intestinal Absorption / Q000187:drug effects* / Q000502:physiology; D007421:Intestine, Small / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis* / Q000378:metabolism; D010477:Perfusion; D011817:Rabbits; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D051269:Sodium-Glucose Transporter 1; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D051272:Glucose Transporter Type 1; D051273:Glucose Transporter Type 2; D007004:Hypoglycemic Agents; D007328:Insulin; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; C495679:Slc2a1 protein, rat; C495676:Slc5a1 protein, rat; D051269:Sodium-Glucose Transporter 1; D012964:Sodium; D005947:Glucose; D020909:Acarbose