Altered lactate metabolism in Huntington's disease is dependent on GLUT3 expression.

Macarena Solís-MaldonadoMaría Paz MiróAníbal I AcuñaAdriana Covarrubias-PintoAnitsi LoaizaGonzalo MayorgaFelipe A BeltránCarlos CepedaMichael S LevineIlona I ConchaLuis Federico BátizMónica A CarrascoMaite A Castro

Published in: CNS neuroscience & therapeutics (2018)

We demonstrate that stimulation of lactate uptake by ascorbic acid is a consequence of inhibiting glucose transport. Supporting this, lactate transport stimulation by ascorbic acid in HD cells was completely restored by overexpressing GLUT3. Therefore, alterations in GLUT3 expression could be responsible for inefficient use of lactate in HD neurons, contributing to the metabolic failure observed in HD.

Keyphrases

poor prognosis
induced apoptosis
signaling pathway
cell cycle arrest
long non coding rna
blood glucose
oxidative stress
blood pressure
cell proliferation
metabolic syndrome
endoplasmic reticulum stress
insulin resistance