Vanadate reduces sodium‐dependent glucose transport and increases glycolytic activity in LLC‐PK1 epithelia

Abstract The effect of vanadate pentoxide on apical sodium‐dependent glucose transport in LLC‐PK1 epithelia was examined. Epithelia grown in the presence or absence of 1 μM vanadate formed confluent monolayers and exhibited no differences in DNA, protein, or ultrastructure. Vanadate‐supplemented epithelia demonstrated a lower steady‐state α‐methyl‐D‐glucopyranoside (AMG) concentrating capacity and a twofold reduction in apical AMG uptake J max . This decreased AMG transport occurred as a consequence of a reduction in the number of transport carriers and was not associated with a change in the sodium electrochemical gradient. The vanadate‐induced reduction in apical glucose carrier functional activity and expression was accompanied by a stimulation of intracellular glycolytic flux activity, as evidenced by increased glucose consumption, lactate production, PFK‐1 activity, and intracellular ATP. There was no difference in intracellular cAMP levels between vanadate‐supplemented and non‐supplemented epithelia. These results demonstrate an association between stimulation of glycolytic pathway activity and an adaptive response in the form of a reduction in the function and expression of the sodium‐dependent apical glucose transporter in LLC‐PK1 epithelia. © 1994 Wiley‐Liss, Inc.