Acute Enterocyte Adaptation to Luminal Glucose: A Posttranslational Mechanism for Rapid Apical Recruitment of the Transporter GLUT2

Abstract

BackgroundGlucose absorption postprandially increases markedly to levels far greater than possible by the classic glucose transporter sodium–glucose cotransporter 1 (SGLT1). HypothesisLuminal concentrations of glucose >50mM lead to rapid, phenotypic, non-genomic adaptations by the enterocyte to recruit another transporter, glucose transporter 2 (GLUT2), to the apical membrane to increase glucose absorption. MethodsIsolated segments of jejunum were perfused in vivo with glucose-containing solutions in anesthetized rats. Carrier-mediated glucose uptake was measured in 10 and 100mM glucose solutions (n = 6 rats each) with and without selective inhibitors of SGLT1 and GLUT2. ResultsThe mean rate of carrier-mediated glucose uptake increased in rats perfused with 100mM versus 10mM glucose to 13.9±2.9 μmol from 2.1±0.1 μmol, respectively (p < 0.0001). Using selective inhibitors, the relative contribution of GLUT2 to glucose absorption was 56% in the 100mM concentration of glucose compared to the 10mM concentration (27%; p < 0.01). Passive absorption accounted for 6% of total glucose absorption at 100mM glucose. ConclusionA small amount of GLUT2 is active at the lesser luminal concentrations of glucose, but when exposed to concentrations of 100 mM, the enterocyte presumably changes its phenotype by recruiting GLUT2 apically to markedly augment glucose absorption.