Triiodothyronine stimulates cystatin C production in bone cells

Thyroid hormones increase cystatin C levels in vivo. To study whether 3,3',5-triiodo-l-thyronine (T(3)) stimulates the production of cystatin C in vitro, we used a T(3)-responsive osteoblastic cell line (PyMS) which can be kept in serum-free culture. We compared the effects of T(3) on cystatin C mRNA expression (by Northern) and on protein release (by Western and ELISA) with those of dexamethasone (dex). Triiodothyronine increased cystatin C mRNA expression and cystatin C accumulation in culture media in a dose- and time-dependent manner, 1.5-fold at 1 nmol/l after 4d; dex (100 nmol/l) was more potent and increased cystatin C accumulation 3-fold after 4d. Triiodothyronine but not dex stimulated glucose uptake. Our in vitro findings explain in vivo observations. Triiodothyronine-induced increase in the production of cystatin C may be related to an increased cell metabolism and proteolysis control demand

Triiodothyronine stimulates glucose transport in bone cells

Thyroid hormones increase energy expenditure and bone turnover in vivo. To study whether 3,3',5-triiodo-l-thyronine (T(3)) stimulates the uptake of glucose in osteoblastic cells, PyMS (a cell line derived from rat bone) cells were kept in serum-free culture medium and treated with T(3). We measured [1-(14)C]-2-deoxy-D: -glucose (2DG) uptake and looked for expression of the high-affinity glucose transporters GLUT1 and GLUT3 by northern and western analysis. T(3) did not influence the cell number but slightly (1.3-fold) increased the protein content of the cell cultures. 2DG uptake was low in serum-deprived cell cultures and was increased by T(3) (up to 2.5-fold at 1 nmol l(-1) after 4 days) in a dose- and time-dependent manner. Triiodothyronine at 1 nmol l(-1) increased GLUT1 and GLUT3 abundance in membranes. Therefore, increased glucose uptake induced by T(3) in osteoblasts may be mediated by the known high-affinity glucose transporters GLUT1 and GLUT3