title: Role of Enhanced Central Leptin Activity in a Scoliosis Model Created in Bipedal Amputated Mice.
abstract: METHODS
  An experimental study to investigate the role of enhanced central leptin activity in a bipedal mouse scoliosis model.
  
  
  OBJECTIVE
  To investigate the influence of enhanced central leptin activity on the development of scoliosis in mice, and to support Burwell's hypothesis that central leptin dysfunction is involved in the etiopathogenesis of idiopathic scoliosis.
  
  
  BACKGROUND
  Significantly lower level of circulating leptin and higher level of soluble leptin receptor have been reported in adolescent idiopathic scoliosis compared with healthy adolescents, suggesting possible association between abnormal central leptin level and dysfunction.
  
  
  METHODS
  Amputation of forelimbs and tail was performed on 50 male C3H/HeJ mice at the age of 3 weeks. Then, the mice were randomly divided into 2 groups: Group A consisted of 25 mice treated with injection into the hypothalamus with lentivirus vectors that overexpressed leptin; and Group B involved the remaining 25 mice receiving intracerebral injection with the control vectors. Radiographs were obtained at 20th week to determine the presence of spinal deformity. The incidence of scoliosis and curve magnitude were compared between groups.
  
  
  RESULTS
  The body weight was initially found to be slightly lower in mice of Group A when compared with Group B. Significantly higher peripheral serum leptin level was found in leptin-overexpressing mice than control mice. Scoliosis developed in 23 mice of Group A (92%), with an average Cobb angle of 30.2°, and in 13 of Group B (52%), with an average Cobb angle of 18.4°, respectively. A higher incidence (P = 0.002) and more severe curve (P <0.001) were observed in Group A.
  
  
  CONCLUSIONS
  In this bipedal mouse scoliosis model, enhanced central leptin activity might not only increase the risk of developing a scoliosis, but also contribute to the progression of scoliosis.
  
  
  METHODS
  N/A.
authors.affiliation: *Department of Spine Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China †Department of Orthopedics, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China ‡The Joint Scoliosis Research Center of Nanjing University and the Chinese University of Hong Kong, Nanjing, China; and §Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Wu
authors.forename: Xu
authors.initials: X
authors.lastname: Sun
authors.forename: Zezhang
authors.initials: Z
authors.lastname: Zhu
authors.forename: Huang
authors.initials: H
authors.lastname: Yan
authors.forename: Jing
authors.initials: J
authors.lastname: Guo
authors.forename: Jack C Y
authors.initials: JC
authors.lastname: Cheng
authors.forename: Yong
authors.initials: Y
authors.lastname: Qiu
mesh_terms: D000671:Amputation, Surgical / Q000379:methods; D000818:Animals; D001835:Body Weight / Q000502:physiology*; D004195:Disease Models, Animal; D018450:Disease Progression; D020738:Leptin / Q000097:blood*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D054411:Receptors, Leptin / Q000378:metabolism; D012306:Risk; D012600:Scoliosis / Q000378:metabolism* / Q000503:physiopathology* / Q000517:prevention & control
chemical_list: D020738:Leptin; D054411:Receptors, Leptin