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Obesity does not affect the healing of femur fractures in mice

机译：肥胖不会影响小鼠股骨骨折的愈合

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Obesity is reported to be both protective and deleterious to bone. Lipotoxicity and inflammation might be responsible for bone loss through inhibition of osteoblasts and activation of osteoclasts. However, little is known whether obesity affects the process of fracture healing. Therefore, we studied the effect of high fat diet-induced (HFD) obesity on callus formation and bone remodelling in a closed femur fracture model in mice. Thirty-one mice were fed a diet containing 60 kJ% fat (HFD) for a total of 20 weeks before fracture and during the entire postoperative observation period. Control mice (n = 31) received a standard diet containing 10 kJ% fat. Healing was analyzed using micro-CT, biomechanical, histomorphometrical, immunohistochemical, serum and protein biochemical analysis at 2 and 4 weeks after fracture. HFD-fed mice showed a higher body weight and increased serum concentrations of leptin and interleukin-6 compared to controls. Within the callus tissue Western blot analyses revealed a higher expression of transcription factor peroxisome proliferator-activated receptor y (PPARy) and a reduced expression of runt-related transcription factor 2 (RUNX2) and bone morphogenetic protein (BMP)-4. However, obesity did not affect the expression of BMP-2 and did not influence the receptor activator of nuclear factor kappa B (RANK)/RANK ligand/osteoprotegerin (OPG) pathway during fracture healing. Although the bones of HFD-fed animals showed an increased number of adipocytes within the bone marrow, HFD did not increase callus adiposity. In addition, radiological and histomorphometric analysis could also not detect significant differences in bone formation between HFD-fed animals and controls. Accordingly, HFD did not affect bending stiffness after 2 and 4 weeks of healing. These findings indicate that obesity does not affect femur fracture healing in mice. (C) 2016 Elsevier Ltd. All rights reserved.
机译：据报道肥胖对骨骼既有保护作用又有害。脂质毒性和炎症可能是通过抑制成骨细胞和激活破骨细胞而导致骨质流失的原因。但是，肥胖对骨折愈合过程的影响知之甚少。因此，我们研究了高脂饮食诱导（HFD）肥胖对小鼠股骨闭合骨折模型中愈伤组织形成和骨重塑的影响。 31只小鼠在骨折前和整个术后观察期内共进食了含60kJ％脂肪（HFD）的饮食，共20周。对照小鼠（n = 31）接受了含10 kJ％脂肪的标准饮食。骨折后2周和4周使用micro-CT，生物力学，组织形态计量学，免疫组织化学，血清和蛋白质生化分析来分析愈合情况。与对照组相比，由HFD喂养的小鼠表现出更高的体重和瘦素和白介素6的血清浓度增加。在愈伤组织中，蛋白质印迹分析显示转录因子过氧化物酶体增殖物激活受体y（PPARy）的表达较高，而矮子相关转录因子2（RUNX2）和骨形态发生蛋白（BMP）-4的表达降低。但是，肥胖在骨折愈合过程中不影响BMP-2的表达，也不影响核因子κB（RANK）/ RANK配体/骨保护素（OPG）途径的受体激活剂。尽管由HFD喂养的动物的骨骼显示出骨髓中脂肪细胞的数量增加，但HFD并未增加愈伤组织的肥胖。另外，放射学和组织形态计量学分析也不能检测到喂食HFD的动物和对照之间的骨形成方面的显着差异。因此，HFD在愈合2周和4周后不会影响弯曲刚度。这些发现表明，肥胖症不会影响小鼠股骨骨折的愈合。 （C）2016 Elsevier Ltd.保留所有权利。

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