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.
These findings may implicate decreases in the number of Purkinje cells and the alterations in the levels of caveolin-1 and synaptotagmin-1 in the impairments of cerebellar development induced by developmental iodine deficiency and hypothyroidism.
On the other hand, hypothyroidism resulted in increased cardiac beta(2)- and beta(3)-adrenoceptor, Gialpha(2), Gialpha(3), GRK3, and eNOS mRNA expressions.
In all, our findings demonstrate that myostatin expression is increased in hypothyroid rats, thus supporting a possible role for this factor in the pathogenesis of the muscle loss that may occur in hypothyroidism.
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.
Strikingly, otoferlin was absent from IHCs of hypothyroid rats but not of Pax8-/- mice, although both cell types showed exocytosis with an efficiency typical for immature IHCs.
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.
One such clone is procollagen lysyl hydroxylase2 (Plod-2), the key enzyme for the first step of collagen biosynthetic pathway, which was down-regulated in hypothyroid condition.