Effect of leptin on bone metabolism in rat model of traumatic brain injury and femoral fracture.

Objective: To observe serum and callus leptin expression within the setting of fracture and traumatic brain injury (TBI).

Methods: A total of 64 male SD rats were randomized equally into 4 groups: nonoperated group, TBI group, fracture group, and fracture+TBI group. Rats were sacrificed at 2, 4, 8 and 12 weeks after fracture+TBI. Serum leptin was detected using radioimmunoassay, and callus formation was measured radiologically. Callus leptin was analyzed by immunohistochemistry.

Results: Serum leptin levels in the fracture group, TBI group and combined fracture+TBI group were all significantly increased compared with control group at the 2 week time-point (P less than 0.05). Serum leptin in the combined fracture +TBI group was significantly higher than that in the fracture and TBI groups at 4 and 8 weeks after injury (P less than 0.05). The percentage of leptin-positive cells in the fracture+TBI callus and callus volume were significantly higher than those in the fracture-only group (P less than 0.01).

Conclusions: We demonstrated elevated leptin expression within healing bone especially in the first 8 weeks in a rat model of fracture and TBI. A close association exists between leptin levels and the degree of callus formation in fractures.