Stimulation of glucose transport in osteoblastic cells by parathyroid hormone and insulin-like growth factor I

Insulin and parathyroid hormone (PTH) regulate glucose metabolism in bone cells. In order to differentiate between the effects of these hormones and to compare the potency of insulin with that of insulin-like growth factor (IGF) I, we treated rat bone-derived osteoblastic (PyMS) cells for different time periods and at different concentrations with insulin, IGF I, or PTH, and measured [1-14C]-2-deoxy-d-glucose (2DG) uptake and incorporation of d-[U-14C] glucose into glycogen. 2DG uptake was Na-independent with an apparent affinity constant (K M) of ~2mmol/l. Expression of the high affinity glucose transporters (GLUT), GLUT1 and GLUT3 but not of GLUT4, was found by Northern and Western analysis. Similar to the findings with primary rat osteoblasts, but distinct from those in rat fibroblasts, 2DG uptake and glycogen synthesis were increased in this cell line after exposure to low concentrations (0.1nmol/l and above) of PTH. IGF I at low doses (0.3nmol/l and above) or insulin at higher doses (1nmol/l and above) stimulated 2DG uptake and [3H] thymidine incorporation into DNA. 2DG transport was enhanced already after 30min of IGF I treatment whereas the effect of PTH became significant after 6h. It is concluded that IGF I rather than insulin may be a physiological regulator of 2DG transport and glycogen synthesis in osteoblast

Stimulation of glucose transport in osteoblastic cells by parathyroid hormone and insulin-like growth factor I

Insulin and parathyroid hormone (PTH) regulate glucose metabolism in bone cells. In order to differentiate between the effects of these hormones and to compare the potency of insulin with that of insulin-like growth factor (IGF) I, we treated rat bone-derived osteoblastic (PyMS) cells for different time periods and at different concentrations with insulin, IGF I, or PTH, and measured [1-(14)C]-2-deoxy-D: -glucose (2DG) uptake and incorporation of D: -[U-(14)C] glucose into glycogen. 2DG uptake was Na-independent with an apparent affinity constant (K (M)) of ~2 mmol/l. Expression of the high affinity glucose transporters (GLUT), GLUT1 and GLUT3 but not of GLUT4, was found by Northern and Western analysis. Similar to the findings with primary rat osteoblasts, but distinct from those in rat fibroblasts, 2DG uptake and glycogen synthesis were increased in this cell line after exposure to low concentrations (0.1 nmol/l and above) of PTH. IGF I at low doses (0.3 nmol/l and above) or insulin at higher doses (1 nmol/l and above) stimulated 2DG uptake and [(3)H] thymidine incorporation into DNA. 2DG transport was enhanced already after 30 min of IGF I treatment whereas the effect of PTH became significant after 6 h. It is concluded that IGF I rather than insulin may be a physiological regulator of 2DG transport and glycogen synthesis in osteoblasts

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