Vanadate reduces sodium-dependent glucose transport and increases glycolytic activity in LLC-PK1 epithelia.
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 microM vanadate formed confluent monolayers and exhibited no differences in DNA, protein, or ultrastructure. Vanadate-supplemented epithelia demonstrated a lower steady-state alpha-methyl-D-glucopyranoside (AMG) concentrating capacity and a twofold reduction in apical AMG uptake Jmax. 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.[1]References
- Vanadate reduces sodium-dependent glucose transport and increases glycolytic activity in LLC-PK1 epithelia. Madsen, K.L., Porter, V.M., Fedorak, R.N. J. Cell. Physiol. (1994) [Pubmed]
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