Growth hormone, somatomedin and cartilage sulfation in failure of catch-up growth after propylthiouracil-induced hypothyroidism in the rat.

Male Long-Evans rats 36 to 39 days of age were fed a diet containing 0.1% propylthiouracil (PTU) for 17 to 20 days followed by the resumption of normal diet. Growth rates of body weight and tail length decreased during PTU treatment and increased during recovery; yet only slight catch-up (compensatory) growth occurred in either body weight or tail length. Although serum thyroxine and triiodothyronine concentrations (radioimmunoassay) decreased significantly during PTU treatment, they returned to normal by recovery day 14. Pituitary immunoassayable growth hormone (GH) content and concentration dropped during PTU-feeding. By recovery day 14 there was significant, but incomplete, repletion of the gland. Serum GH during ether anesthesia was increased significantly during PTU treatment; it remained elevated (NS) and showed greater variability during recovery than in controls. Bioassayable serum somatomedin (Sm) activity decreased during PTU treatment in one of two experiments but returned to a normal level by recovery day 7. The addition of PTU to normal rat serum in concentrations used during PTU treatment failed to alter Sm activity. The addition of L-triiodothyronine and/or L-thyroxine to hypothyroid serum also did not alter Sm activity. In vitro and in vivo cartilage sulfate incorporation decreased during PTU treatment but it rose to greater than control values during the recovery period. The difference in sulfate incorporation between treated and control rats was maintained throughout the observation periods. The results indicate that incomplete catch-up growth following transient hypothyroidism is the result of factors other than deficient GH or Sm production. The implications of the persistent changes in cartilage sulfate metabolism are not clear, but these findings during recovery suggest the possibility that a disturbance of intrinsic cartilage function is a limiting factor preventing full catch-up growth after PTU-induced hypothyroidism.