Insulin and insulin-like growth factor (IGF I) modulate the effects of bTSH on 3H-thymidine incorporation in human thyroid cells in primary culture.

Abstract

The role of TSH in thyroid cell growth and the pathogenesis of goiter has become a matter of recent debate, since many investigators have failed to demonstrate a growth-promoting effect of TSH in human thyroid cells in culture. While those studies have focused on the action of TSH in human thyroid cells, the influence of assay conditions and cofactors has received scant attention. In the present study, we have therefore undertaken to elucidate the effects of insulin and insulin-like growth factor (IGF I) on 3H-thymidine uptake in human thyroid cells, particularly with respect to their relation to the actions of bTSH. We could demonstrate a considerable, dose-dependent stimulation of 3H-thymidine incorporation in the cells by bTSH that was dependent on the presence of insulin or IGF I; bTSH alone was ineffective in that respect. The concentrations of insulin and IGF I required to facilitate the TSH response were of a magnitude at which both peptides were totally ineffective by themselves. At concentrations of insulin or IGF I that produced a maximum stimulation of 3H-thymidine incorporation, the addition of bTSH did result in a slight decrease rather than a further increase of that stimulation. We conclude from these findings, first, that TSH appears to be a growth factor for human thyroid cells under the conditions described, and, second, the effects of TSH on thyroid cell proliferation are under the control of cofactors like insulin and IGF I.