Action of pituitary thyrotropin on the inorganic phosphorous of thyroid tissue in vitro.

Abstract

ADDITION of pituitary thyrotropin (TSH) to the suspending medium effects a variety of changes in the intermediary metabolism of surviving thyroid tissue1. In attempting to characterize the biochemical attributes of this transition from ‘rest’ to ‘work’ distinction has been made between the changes which can be demonstrated in simple saline media devoid of organic metabolites, and those which occur in media which have been supplemented with potential exogenous substrates such as glucose2. It has been proposed that the unsupplemented systems unmask intrathyroidal realignments for the initiation of ‘work’ from endogenous resources, while the supplemented systems reflect assimilative alterations for sustaining ‘work’ through an exogenous renewal of substrate1,2. In a forthcoming review, it has been suggested that the endogenous priming results from the simultaneous occurrence of multiple catabolic events within the thyroid1. Thus, the virtually immediate effects of TSH to: (a) promote thyroidal Qo2 in unsupplemented systems3; (b) increase intrathyroidal free sialic acid4; (c) liberate free amino-acids from thyroglobulin5 might reflect concurrent (a) mobilization of preformed endogenous substrates, as well as an activation of intrathyroidal (b) neuraminidases and glycosidases, and (c) proteases and peptidases. The more recent demonstrations that TSH may augment glyco-genolysis in thyroid slices6 and directly enhance intrathyroidal proteolysis in vitro7 afford further examples of essentially catabolic components in the initial ‘work’ response. In view of these considerations, it was considered desirable to re-examine our earlier observations that TSH can increase intrathyroidal inorganic phosphorus (Pin) in unsupplemented systems3.