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首页> 外文期刊>Cellular Physiology and Biochemistry >Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/?2-Catenin in Rats
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Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/?2-Catenin in Rats

机译：糖尿病通过调节Sema3A / IGF-1 /？2-catenin扰动大鼠骨骼的微结构和骨骼强度

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>Purpose: Increasing evidence supported that semaphorin 3A (Sema3A), insulin-like growth factor (IGF)-1 and ?2-catenin were involved in the development of osteoporosis and diabetes. This study is aimed to evaluate whether Sema3A/IGF-1/?2-catenin is directly involved in the alterations of bone microarchitecture and bone strength of diabetic rats. Methods: Diabetic rats were induced by streptozotocin and high fat diet exposure. Bone microarchitecture and strength in the femurs were evaluated by micro-CT scanning, three-point bending examination and the stainings of HE, alizarin red S and safranin O/fast green, respectively. The alterations of lumbar spines microarchitecture were also determined by micro-CT scanning. Western blot and immunohistochemical analyses were used to examine the expression of Sema3A, ?2-catenin, IGF-1, peroxisome proliferator-activated receptor ?3 (PPAR?3) and cathepsin K in rat tibias. Results: Diabetic rats exhibited decreased trabecular numbers and bone formation, but an increased trabecular separation in the femurs and lumbar spines. Moreover, the increased bone fragility and decreased bone stiffness were evident in the femurs of diabetic rats. Diabetic rats also exhibited a pronounced bone phenotype which manifested by decreased expression of Sema3A, IGF-1 and ?2-catenin, as well as increased expression of cathepsin K and PPAR?3. Conclusions: This study suggests that diabetes could perturb bone loss through the Sema3A/IGF-1/?2-catenin pathway. Sema3A deficiency in bone may contribute to upregulation of PPAR?3 and cathepsin K expression, which further disrupts bone remodeling in diabetic rats.
机译：> 目的： 越来越多的证据支持semaphorin 3A（Sema3A），胰岛素样生长因子（IGF）-1和β2-catenin参与了Sph的发展。骨质疏松症和糖尿病。本研究旨在评估Sema3A / IGF-1 /β2-catenin是否直接参与糖尿病大鼠骨微结构和骨强度的改变。 方法： 链脲佐菌素和高脂饮食暴露可诱发糖尿病大鼠。通过显微CT扫描，三点弯曲检查以及HE，茜素红S和番红O /坚牢绿的染色来评估股骨的骨微结构和强度。腰椎微结构的改变也通过微CT扫描确定。用Western印迹和免疫组化分析检查大鼠胫骨中Sema3A，α2-连环蛋白，IGF-1，过氧化物酶体增殖物激活受体β3（PPARβ3）和组织蛋白酶K的表达。 结果： 糖尿病大鼠的小梁数目和骨形成减少，但股骨和腰椎的小梁间距增加。此外，在糖尿病大鼠的股骨中，骨脆性增加和骨刚度降低是明显的。糖尿病大鼠还表现出明显的骨表型，其表现为Sema3A，IGF-1和β2-catenin的表达降低，以及组织蛋白酶K和PPARβ3的表达增加。 结论： 这项研究表明，糖尿病可以通过Sema3A / IGF-1 /？2-catenin途径干扰骨质流失。骨骼中Sema3A缺乏可能导致PPAR？3和组织蛋白酶K表达上调，这进一步破坏了糖尿病大鼠的骨骼重塑。

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