Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and
attenuates structural remodeling in pressure overload but does not prevent left
ventricular dysfunction.
Authors Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Anderson SM, Abel ED
Submitted By E. Dale Abel on 4/15/2014
Status Published
Journal Journal of the American Heart Association
Year 2013
Date Published 10/1/2013
Volume : Pages 2 : e000301
PubMed Reference 24052497
Abstract Increased glucose transporter 1 (GLUT1) expression and glucose utilization that
accompany pressure overload-induced hypertrophy (POH) are believed to be
cardioprotective. Moreover, it has been shown that lifelong transgenic
overexpression of GLUT1 in the heart prevents cardiac dysfunction after aortic
constriction. The relevance of this model to clinical practice is unclear
because of the life-long duration of increased glucose metabolism. Therefore, we
sought to determine if a short-term increase in GLUT1-mediated myocardial
glucose uptake would still confer cardioprotection if overexpression occurred at
the onset of POH.

Investigators with authorship
E. Dale AbelUniversity of Iowa