In all, our data show that the regulation of GLUT1 and GLUT3 in cerebral cortex is regulated by T(3) in a complex way and suggest that alterations in the expression of glucose transporters induced by hypothyroidism might have a functional impact on brain glucose uptake.
In this study, we demonstrated that hypothyroidism stimulated, while hyperthyroidism suppressed, PC1 mRNA levels in rat hypothalamus and cerebral cortex, but not in hippocampus.
In mitochondria from hypothyroid rats, the changes in catalytic activities of F0F1-ATP synthase are accompanied by a decrease in the amount of immunodetected beta-F1, F0 1-PVP, and OSCP subunits of the complex.
The present study reveals that the reduced Pitx2 expression in hypothyroid ovary could lead to ovarian dysfunction by modulating the Pitx2-Plod2 interaction, further study will be necessary to unravel the complete regulatory mechanism of Pitx2 in ovarian function.
Western blotting showed reduction in phosphorylated (P)-CAMKII, total-CaMKII, neurogranin, and calmodulin basal levels in the CA1 region of the hippocampus of hypothyroid rats.
The role of thyroid hormone (TH) in the expression of neurofilament (NF) genes during the first 3-4 postnatal weeks of rat brain development has been examined.I.p. administration of TH to 2-day-old hypothyroid rats resulted in a 2-fold increase in cerebral NF-M and NF-L mRNAs, while administration to 15-day-old hypothyroid rats led to a 1.5- to 3-fold increase in NF-H mRNA within 2-4 h of hormone injection.
The role of thyroid hormone (TH) in the expression of neurofilament (NF) genes during the first 3-4 postnatal weeks of rat brain development has been examined.I.p. administration of TH to 2-day-old hypothyroid rats resulted in a 2-fold increase in cerebral NF-M and NF-L mRNAs, while administration to 15-day-old hypothyroid rats led to a 1.5- to 3-fold increase in NF-H mRNA within 2-4 h of hormone injection.
We tested whether steroid receptor coactivator-1 (SRC-1) and nuclear corepressor (N-CoR) expression is altered by hypothyroidism in rat brains on gestational day 16 and postnatal day 15.
Developmental hypothyroidism induced by iodine deficiency and PTU treatment could delay the maturation of newborn granule neurons in dentate gyrus, and this deficit may be attributed to the downregulation of p35.
Primary rat pituitary cells cultures from hypo- and euthyroid rats in the presence of actinomycin D showed that hypothyroidism increased the half-life of PAM mRNA from 9-10 h to 15-17 h. Taken together, these data suggest that hypothyroidism induces PAM mRNA levels by increasing its stability in the cytoplasm.