Objective: Thiazolidinediones offer promise as oral insulin-sensitizing agents. Peroxisome proliferator-activated receptor-g (PPARg), a member of the steroid receptor superfamily, play a pivotal role in the differentiation of adipocytic cells. Osteoblasts and adipocytes are derived from common bone marrow stromal cells that play crucial roles in the generation of osteoclasts. Activation of peroxisome proliferator-activated receptor-g (PPARg) induces adipogenic differentiation of stromal cells. Effects of rosiglitazone on osteoblasts/osteoclast differention is unknown. The aim of this study was to examine rosiglitazone effects on bone strength in ovariectomized (OVX) rats.
Methods: Thirthy-six Spraque-Dawney rats were used to study the effects of rosiglitazone. Experimental group included: (1) OVX plus rosiglitazone (1mg/kg daily po by gavage), (2) OVX plus vechile, (3) sham OVX. Treatment was initiated 12 weeks after ovariectomy and continued for 6 weeks. The effects of ovx, rosiglitazone were measured at femur and lumbal vertebras (L4). Bone strength was assessed with compression test in vertebras and with three-point bending test in femurs by using Shimadzu AG-50 kNG as newton (N). Statistical analyses made by Mann-Whitney U nonparametric test, correlation analysis and Kruskal Wallis test.
Results: It was shown that rosiglitazone increases femoral and vertebral bone strength in osteoporotic rats. But, there is no statistically significant in vertebras analyses whereas is significant differences in femurs analyses. Bone strength was found to be 87,3±28,6 N in femurs of OVX plus rosiglitazone and 70,7± 13,4 N in femurs of osteoporotic rats (p=0.04) whereas 121,6± 32,1 N in vertebras of the OVX plus rosiglitazone and 107,43±28,89 N in vertebras of OVX group (p=0,058).
Conclusion: Rosiglitazone may suppress bone resorption and prevent bone loss. In this study, the use of rosiglitazone was associated with increase of femoral bone strength significantly osteoporotic rats, but not significantly in vertebral.
08 - 11 Apr 2002
British Endocrine Societies