Effect and mechanism of leptin on bone metabolism in postmenopausal women

Abstract

Objective To investigate the effects of Leptin on the base of anthropometry, densitometry, and biochemistry and reveal the role of Leptin in bone metabolism in postmenopausal women with osteoporosis (OP). Methods From January 2008 to January 2014, data of 82 postmenopausal females with or without OP were analyzed. They were randomized into two groups: OP (n=40) and conditional control group (CON) (n=42). The expression of Leptin receptors in osteoblasts was observed by immunohistochemistry. 1×10 ng/ml, 1×102 ng/ml, 1×103 ng/ml, 1×104 ng/ml of Leptin were added respectively. Then the proliferation, differentiation and mineralization of osteoblasts were measure at 24 h, 48 h and 96 h. The gene expressions of bone marrow mesenchymal stem cells (BMSCs) derived osteoblasts and adipocytes treated with Leptin were examined by quantitative analysis of Real time-PCR. Results The expression of Leptin receptors in osteoblasts was observed on plasma membranes and cytoplasm in the normal group and osteoporosis group. In osteoporosis group, different concentrations of Leptin enhanced cell proliferation, cell differentiation and cell mineralization. The growth rate of MTT and the concentration of ALP in the serum of were significantly increased with the effects of 1×10 ng/ml, 1×102 ng/ml and 1×103 ng/ml of Leptin, and the action of 1×102 ng/ml Leptin was the most powerful with time dependence. Within 96 hours, the growth rate of osteoblasts increased gradually, and the concentration of ALP increased gradually in 3 weeks. The expression of RANKL/OPG in bone marrow BMSCs derived osteoblasts treated with Leptin were significantly increased. Conclusion Leptin receptor is present in osteoblasts, and Leptin affects biological behaviors of osteoblasts through receptors. The direct effect of Leptin may relate the expression of RANKL/OPG. Then, the balance between bone resorption and bone formation was broken and finally osteoporosis occurred. Lepin may promote osteogenesis and inhibit bone resorption in the differentiation of BMSCs. Key words: Osteoporosis, postmenopausal; Leptin; Bone diseases, metabolic