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Abstract:
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Pyridoxine-deficient young rats (3 weeks old) had
significantly reduced levels of pituitary TSH, serum
thyroxine (T4) and tri iodothyn nine (T,,) Compared
with pyridoxine-supplemented rats. The status of the
pituitary-thyroid axis of normal, pyridoxine-supplemented
and pyridoxine-deficient rats was evaluated
by studying the binding parameters of [3H](3-nicthylhistidine2)
TRH in the pituitary of these rats. The
effects of TRH and 1'4 injections on pituitary TSH
and serum TSH, T4 and T3 of these two groups were
also compared. The maximal binding of TRH receptors
in the pituitary of pyridoxine-deficient rats was
significantly higher than that of pyridoxine-supplemented
control and normal rats, but there was no change in the binding affinity. Treatment with TRH
stimulated TSH synthesis and release. It also
increased serum T4 and T3 in both pyridoxine-supplemented
and pyridoxine-deficient rats. Treatment with
T4 decreased serum and pituitary TSH in both
pyridoxine-supplemented and pyridoxine-deficient
rats, compared with saline-treated rats. The increased
pituitary TRH receptor content, response to TRH
administration and the fact that regulation at the level
of the pituitary is not affected in the pyridoxinedeficient
rat indicates a hypothalamic origin for the
hypothyroidism of the pyridoxine-deficient rat. |