The adaptation of TSH secretion to autonomy in non-toxic goiter may be based-on active regulation of set-point and sensitivity of central TSH-receptors, perhaps by the microRNA (MIR) gene.

摘要

The hypothalamic-pituitary-thyroid (HPT) feedback system is one of the most complex regulatory systems and it has intrigued researchers for more than 50 years. One of the unsolved problems of this regulation in humans is the hypothalamic and pituitary adaption to autonomous function of the thyroid gland in non-toxic goiter (NTG). A new hypothesis, that TSH secretion is actively regulated in NTG in response to changes in thyroid autonomy in order to keep the patient euthyroid, was discussed in the present study on basis of previous experimental data in NTG patients with different degree of autonomous function. The patients were submaximally suppressed for one month with a fixed daily dose of T3. Group data suggested an inverse correlation between TSH suppression and suppression of thyroid function. Group data also suggested that TSH suppression was significantly correlated to basal TSH. This means that a NTG patient with a low normal TSH in blood before suppression (basal TSH) and a high degree of autonomous function may exhibit a relatively high TSH suppression. This ensures a minimal stimulation of the thyroid gland thereby protecting the gland from developing hyperthyroidism. A patient with a high normal TSH in blood before suppression (basal TSH) and a low degree of autonomous function, may exhibit a relatively low TSH suppression, indicating a high stimulation of the thyroid gland thereby protecting the patient from developing hypothyroidism. It is hypothesized that this adaption of TSH secretion to autonomy in NTG patients may be based on active regulation of both the set- point of the central TSH-receptors and the sensitivity of these receptors as well. Such an active regulation of the HPT axis may be controlled by one of the newly found post-transcriptional genes called MIR (microRNA).