Effect of Primary Congenital Hypothyroidism upon Expression of Genes Mediating Murine Brain Glucose Uptake View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-05

AUTHORS

Janine Y Khan, Rosario A Rajakumar, Uday P Devaskar, Lisa A Weissfeld, Sherin U Devaskar

ABSTRACT

Using hyt/hyt mice that exhibit naturally occurring primary hypothyroidism (n = 72) and Balb/c controls (n = 66), we examined the mRNA, protein, and activity of brain glucose transporters (Glut 1 and Glut 3) and hexokinase I enzyme at various postnatal ages (d 1, 7, 14, 21, 35, and 60). The hyt/hyt mice showed an age-dependent decline in body weight (p < 0.04) and an increase in serum TSH levels (p < 0.001) at all ages. An age-dependent translational/posttranslational 40% decline in Glut 1 (p = 0.02) with no change in Glut 3 levels was observed. These changes were predominant during the immediate neonatal period (d 1). A posttranslational 70% increase in hexokinase enzyme activity was noted at d 1 alone (p < 0.05) with no concomitant change in brain 2-deoxy-glucose uptake. This was despite a decline in the hyt/hyt glucose production rate. We conclude that primary hypothyroidism causes a decline in brain Glut 1 associated with no change in Glut 3 levels and a compensatory increase in hexokinase enzyme activity. These changes are pronounced only during the immediate neonatal period and disappear in the postweaned stages of development. These hypothyroid-induced compensatory changes in gene products mediating glucose transport and phosphorylation ensure an adequate supply of glucose to the developing brain during transition from fetal to neonatal life. More... »

PAGES

718-725

References to SciGraph publications

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  • 1996-09. Fuel Utilization by Early Newborn Brain Is Preserved under Congenital Hypothyroidism in the Rat in PEDIATRIC RESEARCH
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  • 1994-09. Delayed Ultrastructural Lung Maturation in the Fetal and Newborn Hypothyroid (Hyt/Hyt) Mouse in PEDIATRIC RESEARCH
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1203/00006450-199905010-00019

    DOI

    http://dx.doi.org/10.1203/00006450-199905010-00019

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1064216354

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/10231871


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    38 schema:description Using hyt/hyt mice that exhibit naturally occurring primary hypothyroidism (n = 72) and Balb/c controls (n = 66), we examined the mRNA, protein, and activity of brain glucose transporters (Glut 1 and Glut 3) and hexokinase I enzyme at various postnatal ages (d 1, 7, 14, 21, 35, and 60). The hyt/hyt mice showed an age-dependent decline in body weight (p < 0.04) and an increase in serum TSH levels (p < 0.001) at all ages. An age-dependent translational/posttranslational 40% decline in Glut 1 (p = 0.02) with no change in Glut 3 levels was observed. These changes were predominant during the immediate neonatal period (d 1). A posttranslational 70% increase in hexokinase enzyme activity was noted at d 1 alone (p < 0.05) with no concomitant change in brain 2-deoxy-glucose uptake. This was despite a decline in the hyt/hyt glucose production rate. We conclude that primary hypothyroidism causes a decline in brain Glut 1 associated with no change in Glut 3 levels and a compensatory increase in hexokinase enzyme activity. These changes are pronounced only during the immediate neonatal period and disappear in the postweaned stages of development. These hypothyroid-induced compensatory changes in gene products mediating glucose transport and phosphorylation ensure an adequate supply of glucose to the developing brain during transition from fetal to neonatal life.
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