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1 Division of Neonatology and Developmental Biology, Department of Pediatrics, Magee-Womens Research Institute, University of Pittsburgh, Pittsburgh, Pennsylvania 15213; 2 Division of Neonatology, Department of Pediatrics, Health Sciences Center, St. Louis University, St. Louis, Missouri 63104; and 3 Division of Neonatology, Department of Pediatrics, University of Colorado, Denver, Colorado 80217
To determine the cellular adaptations to
fetal hyperglycemia and hypoglycemia, we examined the time-dependent
effects on basal (GLUT-1 and GLUT-3) and insulin-responsive (GLUT-4)
glucose transporter proteins by quantitative Western blot analysis in
fetal ovine insulin-insensitive (brain and liver) and insulin-sensitive
(myocardium, skeletal muscle, and adipose) tissues. Maternal glucose
infusions causing fetal hyperglycemia resulted in a transient 30%
increase in brain GLUT-1 but not GLUT-3 levels and a decline in liver
and adipose GLUT-1 and myocardial and skeletal muscle GLUT-1 and GLUT-4 levels compared with gestational age-matched controls. Maternal insulin
infusions leading to fetal hypoglycemia caused a decline in brain
GLUT-3, an increase in brain GLUT-1, and a subsequent decline in liver GLUT-1, with no significant change in
insulin-sensitive myocardium, skeletal muscle, and adipose tissue
GLUT-1 or GLUT-4 concentrations, compared with gestational age-matched
sham controls. We conclude that fetal glucose transporters are subject
to a time-dependent and tissue- and isoform-specific differential
regulation in response to altered circulating glucose and/or
insulin concentrations. These cellular adaptations in GLUT-1 (and
GLUT-3) are geared toward protecting the conceptus from perturbations
in substrate availability, and the adaptations in GLUT-4 are geared
toward development of fetal insulin resistance.
maternal diabetes; maternal hyperglycemia; maternal hypoglycemia; fetal hyperglycemia; fetal hypoglycemia
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