|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
5 Pt 1
|
|
pubmed:dateCreated |
1999-6-28
|
|
pubmed:abstractText |
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.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 3,
http://linkedlifedata.com/resource/pubmed/chemical/Hexokinase,
http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thyrotropin,
http://linkedlifedata.com/resource/pubmed/chemical/Slc2a1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Slc2a3 protein, mouse
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
May
|
|
pubmed:issn |
0031-3998
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
45
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
718-25
|
|
pubmed:dateRevised |
2007-11-14
|
|
pubmed:meshHeading |
pubmed-meshheading:10231871-Aging,
pubmed-meshheading:10231871-Amino Acid Substitution,
pubmed-meshheading:10231871-Animals,
pubmed-meshheading:10231871-Animals, Newborn,
pubmed-meshheading:10231871-Brain,
pubmed-meshheading:10231871-Congenital Hypothyroidism,
pubmed-meshheading:10231871-Female,
pubmed-meshheading:10231871-Glucose Transporter Type 1,
pubmed-meshheading:10231871-Glucose Transporter Type 3,
pubmed-meshheading:10231871-Hexokinase,
pubmed-meshheading:10231871-Hypothyroidism,
pubmed-meshheading:10231871-Male,
pubmed-meshheading:10231871-Mice,
pubmed-meshheading:10231871-Mice, Inbred BALB C,
pubmed-meshheading:10231871-Mice, Knockout,
pubmed-meshheading:10231871-Monosaccharide Transport Proteins,
pubmed-meshheading:10231871-Nerve Tissue Proteins,
pubmed-meshheading:10231871-Protein Processing, Post-Translational,
pubmed-meshheading:10231871-RNA Processing, Post-Transcriptional,
pubmed-meshheading:10231871-Receptors, Thyrotropin
|
|
pubmed:year |
1999
|
|
pubmed:articleTitle |
Effect of primary congenital hypothyroidism upon expression of genes mediating murine brain glucose uptake.
|
|
pubmed:affiliation |
Department of Pediatrics, University of Pittsburgh School of Medicine, PA 15213, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
