Role of high central leptin activity in a scoliosis model created in bipedal amputated mice

Significantly lower circulating leptin level has been reported in adolescent idiopathic scoliosis (AIS) compared to healthy adolescents. It was hypothesized that leptin dysfunction might be involved in the etiopathogenesis of AIS. In this study, a scoliosis model of bipedal amputated mice with high central leptin activity was established to validate this hypothesis. Three days after bipedal amputation, the mice were randomly divided into two groups: then 8 mice were injected in the hypothalamus with lentivirus vectors which expressed leptin, whereas the remaining 8 were injected with lentivirus vectors expressing GFP (control vector). X-rays were obtained at 20th week to determine the development of spinal deformity. After that all mice were sacrificed, and blood samples were collected. Then peripheral leptin levels were measured by an ELISA kit. Comparisons for the incidence of scoliosis and the severity of the curves were performed between groups. The body weight was found to be slightly lower in the leptin-vector-treated C3H/HeJ mice when compared with control mice. Significantly higher peripheral serum leptin level was found in leptin-vector-treated mice than control mice. Scoliosis was observed in all leptin-vector-treated mice with an average Cobb angle of 28.2°, and in 4/8 of control with an average Cobb angle of 23.5°. The incidence of scoliosis was significantly higher in leptin-vector-treated mice than in control group, although no significant difference was found in terms of curve severity. The results of this study indicated that the high central leptin activity might not only increase the risk of developing a scoliosis in bipedal mice but also contribute to the progression of scoliosis. The high central leptin activity might play an important role in the etiopathogenesis of scoliosis.