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J Biol Chem, Vol. 274, Issue 25, 17626-17634, June 18, 1999
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From the Glucose constitutes a major fuel for the heart,
and high glucose uptake during fetal development is coincident with the
highest level of expression of the glucose transporter GLUT-1 during
life. We have previously reported that GLUT-1 is repressed perinatally in rat heart, and GLUT-4, which shows a low level of expression in the
fetal stage, becomes the main glucose transporter in the adult. Here,
we show that the perinatal expression of GLUT-1 and GLUT-4 glucose
transporters in heart is controlled directly at the level of gene
transcription. Transient transfection assays show that the Departament de Bioquímica i Biologia
Molecular, Facultat de Biologia, Diagonal 645, Universitat de
Barcelona, Barcelona 08028, Spain, the ¶ Molecular Cardiology
Unit, Laboratory of Cardiovascular Science, Gerontology Research
Center, NIA, National Institutes of Health,
Baltimore, Maryland 21224, and the Cardiothoracic Surgery,
National Heart and Lung Institute, Imperial College School of Medicine,
Dovehouse St., London SW3 6LY, United Kingdom
99/33
fragment of the GLUT-1 gene is sufficient to drive
transcriptional activity in rat neonatal cardiomyocytes. Electrophoretic mobility shift assays demonstrate that the
transcription factor Sp1, a trans-activator of
GLUT-1 promoter, binds to the 102/82 region of
GLUT-1 promoter during the fetal state but not during
adulthood. Mutation of the Sp1 site in this region demonstrates that
Sp1 is essential for maintaining a high transcriptional activity in
cardiac myocytes. Sp1 is markedly down-regulated both in heart and in
skeletal muscle during neonatal life, suggesting an active role for Sp1
in the regulation of GLUT-1 transcription. In all, these
results indicate that the expression of GLUT-1 and GLUT-4 in heart
during perinatal development is largely controlled at a transcriptional
level by mechanisms that might be related to hyperplasia and that are
independent from the signals that trigger cell hypertrophy in the
developing heart. Furthermore, our results provide the first functional
insight into the mechanisms regulating muscle GLUT-1 gene
expression in a live animal.
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