Influence of hypothyroidism on growth hormone binding by rat liver

The binding of 125I-iodinated human GH ([125I]iodo-hGH) to crude, membrane-rich preparations from the livers of thyroidectomized male rats was examined to determine if alterations in GH binding might explain hypothyroid-induced growth failure. Membrane preparations from chronically hypothyroid rats bound nearly twice as much labeled hGH (12.8 +/- 2.5%; mean +/- 1 SD) as those from normal rats (6.6 +/- 1.4%) or thyroxine-treated thyroidectomized animals (7.0 +/- 1.1%). Binding by membrane preparations from hypothyroid rats treated with hGH for 2 weeks was 12.3%. By Scatchard analysis the apparent affinities of the membrane preparations for hGH were relatively constant (Ka = 2.30-2.88 X 10(9) M-1) among the experimental groups. Ovine PRL was only 1.4% as potent as hGH in displacing [125I]iodo-hGH from the liver preparations, indicating that hGH was bound primarily to somatogenic sites. Since administration of hGH did not reduce the binding of [125I]iodo-hGH, it is unlikely that the increase in hGH binding in hypothyroidism is mediated by a reduction in the ambient GH concentration. Furthermore, this increase in [125I]iodo-hGH binding indicates that an alteration in binding of GH to its receptor probably does not mediate either the low somatomedin levels or the growth failure that result from hypothyroidism.