摘要：SummaryIncreased consumption of fats and added sugars has been associated with an increase in metabolic syndromes. Here we show that mice chronically fed an energy-rich diet (ERD) with high fat and moderate sucrose have enhanced the absorption of a gastrointestinal fructose load, and this required expression of the arrestin domain protein Txnip in the intestinal epithelial cells. ERD feeding induced gene and protein expression of Glut5, and this required the expression of Txnip. Furthermore, Txnip interacted with Rab11a, a small GTPase that facilitates the apical localization of Glut5. We also demonstrate that ERD promoted Txnip/Glut5 complexes in the apical intestinal epithelial cell. Our findings demonstrate that ERD facilitates fructose absorption through a Txnip-dependent mechanism in the intestinal epithelial cell, suggesting that increased fructose absorption could potentially provide a mechanism for worsening of metabolic syndromes in the setting of a chronic ERD.Graphical AbstractDisplay OmittedHighlights•Consumption of energy-rich diets (ERDs) promotes intestinal fructose absorption•Intestinal Txnip is required for increased fructose absorption by ERD•Txnip increases fructose transporter Glut5 protein and gene expression•Txnip forms a complex with Rab11a to facilitate the apical localization of Glut5Human Metabolism; Molecular Biology
