Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta.
J Endocrinol
; 163(3): 385-94, 1999 Dec.
Article
em En
| MEDLINE
| ID: mdl-10588811
ABSTRACT
The influence of maternal hypothyroxinemia on the expression of the glucose transporters, GLUT1 and GLUT3, in rat fetal brain and placenta was investigated. Fetal growth was retarded in hypothyroxinemic pregnancies, but only before the onset of fetal thyroid hormone synthesis. Placental weights were normal, but placental total protein concentration was reduced at 19 days gestation (dg). Immunoblotting revealed a decreased abundance of GLUT1 in placental microsomes at 16 dg, whereas GLUT3 was increased. Fetal serum glucose levels were reduced at 16 dg. In fetal brain, the concentration of microsomal protein was deficient at 16 dg and the abundance of parenchymal forms of GLUT1 was further depressed, whereas GLUT3 was unaffected. Northern hybridization analysis demonstrated normal GLUT1 mRNA levels in placenta and fetal brain. In conclusion, maternal hypothyroxinemia results in fetal growth retardation and impaired brain development before the onset of fetal thyroid function. Glucose uptake in fetal brain parenchyma may be compromised directly, due to deficient GLUT1 expression in this tissue, and indirectly, as a result of reduced placental GLUT1 expression. Though corrected by the onset of fetal thyroid hormone synthesis, these deficits are present during the critical period of neuroblast proliferation and may contribute to long term changes in brain development and function seen in this model and in the progeny of hypothyroxinemic women.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Placenta
/
Encéfalo
/
Proteínas de Transporte de Monossacarídeos
/
Retardo do Crescimento Fetal
/
Hipotireoidismo
/
Proteínas do Tecido Nervoso
Limite:
Animals
/
Pregnancy
Idioma:
En
Revista:
J Endocrinol
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
Reino Unido