A potential novel mechanism for precocious puberty in juvenile hypothyroidism

J Clin Endocrinol Metab. 1995 Jan;80(1):276-9. doi: 10.1210/jcem.80.1.7829625.


Some children with juvenile hypothyroidism exhibit unexplained precocious puberty. Interaction of TSH with the human FSH receptor (hFSH-R) is a possible pathophysiological mechanism for this syndrome that has not been explored due to the lack of hFSH-free TSH preparations and the scarcity of a suitable hFSH-R-based assay system. To devise an in vitro FSH bioassay suitable for exploring this mechanism, we expressed hFSH-R complementary DNA in COS-7 cells and stimulated them with recombinant hTSH (rec-hTSH). Rec-hTSH elicited a dose-dependent cAMP response in the in vitro hFSH-R bioassay; however, the concentration of rec-hTSH required for half-maximal stimulation was several logs greater than that of hFSH. Rec-hTSH acted as a competitive inhibitor of hFSH at the hFSH-R, indicating that hTSH and hFSH are acting through the same receptor, namely the hFSH-R. This provides a potential novel mechanism for the precocious puberty of juvenile hypothyroidism.

MeSH terms

  • Biological Assay
  • Cell Line
  • Cyclic AMP / metabolism
  • Dose-Response Relationship, Drug
  • Follicle Stimulating Hormone / antagonists & inhibitors
  • Follicle Stimulating Hormone / pharmacology
  • Humans
  • Hypothyroidism / complications*
  • Puberty, Precocious / etiology*
  • Receptors, FSH / drug effects
  • Receptors, FSH / genetics
  • Receptors, FSH / physiology
  • Recombinant Proteins
  • Thyrotropin / pharmacology*
  • Transfection


  • Receptors, FSH
  • Recombinant Proteins
  • Follicle Stimulating Hormone
  • Thyrotropin
  • Cyclic AMP