Abstract
In this study, our objective was to evaluate effects of leptin on fracture healing in rats. Seventy two male Sprague-Dawley (SD) rats were randomized into 3 groups. Standardized femoral fractures were created in all the rats. Group A was treated with 1 mL normal saline (NS), group B with 0.3 μg/kg leptin in 1 mL NS, and group C with 0.5 μg/kg leptin in 1 mL NS for 2 weeks intraperitoneally. Each group was divided into three subgroups including 8 rats for evaluation at 2, 4 and 8 weeks. Radiological evaluation showed that callus formation of group B and C was all significantly higher than group A at 8 weeks (P=0.04 and P=0.013, respectively). There was no statistically significant difference in fracture healing between group B and group C at 8 weeks (P=0.197). Histological evaluation revealed fracture healing of group B and C was better than group A at 4 weeks (P=0.01 and P=0.002, respectively) and 8 weeks (P=0.008 and P=0.003, respectively). Micro-computed tomography (Micro-CT) analysis demonstrated that greater amounts of bony callus and evidence of bone fusion were observed in group B and C at 4 weeks (P=0.02 and P=0.04, respectively) and 8 weeks (P=0.005 and P=0.001, respectively) compared to group A. Group C also had better fracture healing than group B at 8 weeks (P=0.01). In conclusion, leptin has a positive effect on rat femoral fracture healing.
Highlights
Leptin is a peptide hormone which is secreted especially by white adipose tissue and encoded by the obese gene
At 2 weeks after operation, evidence of callus formation was found at the fracture site in these groups, but there was no statistically significant difference
At 4 weeks after operation, callus formation in the three groups was more rapid and the average evaluation scores were higher than 2 weeks; we did not detect significant difference in these groups
Summary
Leptin is a peptide hormone which is secreted especially by white adipose tissue and encoded by the obese gene. It is produced primarily by adipocytes and acts on the hypothalamus. The role of leptin in bone metabolism has been identified[2-3]. The role of leptin on the skeletal system is complex. Present information on leptin indicates that it is involved in at least 2 different bone-controlling mechanisms, a direct stimulatory effect on bone growth, and/or an indirect suppressive effect on bone formation through the hypothalamus via the sympathetic nervous system[4]. By acting on the hypothalamus and increasing both sympathetic output, and β2-adrenergic receptors on the surface of osteoblasts, leptin exerts an antiosteogenic effect on the central nervous system[5]
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