Endocrine Abstracts

T3 is essential for normal skeletal development. Childhood hypothyroidism causes delayed bone formation, whereas T3-excess accelerates growth and epiphyseal closure. Fibroblast growth factors (FGFs) act via receptor tyrosine kinases (FGFRs) to inhibit chondrocyte proliferation, matrix production and skeletal maturation. Dimerisation of FGFRs and their functional interaction with FGFs requires heparan sulphate proteoglycans (HSPGs). We recently showed that T3 induces FGFR-1 exp...

Studies of TSHR−/− mice suggest that TSH inhibits bone turnover, but these mice have congenital hypothyroidism and the actions of TSH cannot be separated from effects of thyroid hormone deficiency. We characterised skeletal development in hyt/hyt mice, which have a point mutation in the Tshr gene, and Pax8−/− mice with thyroid gland agenesis. Hyt/hyt mice have a 100-fold increase in TSH but inactive TSHRs, whereas Pax8&...