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首页> 外文期刊>Journal of Cellular Physiology >Both spontaneous Ins2+/- and streptozotocin-induced type I diabetes cause bone loss in young mice
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Both spontaneous Ins2+/- and streptozotocin-induced type I diabetes cause bone loss in young mice

机译：和自发isn2 + / -体外实验I型糖尿病引起骨损失在年轻的老鼠

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The adolescent skeleton undergoes accelerated growth determining overall bone density, length, and quality. Diseases such as type 1 diabetes (T1D), most often diagnosed in adolescents, can alter bone processes and promote bone loss. Studies examining type 1 diabetic (T1D) bone pathologies typically utilize adult mice and rely on pharmacologic models such as streptozotocin (STZ)-induced diabetic rodents. To test the effect of T1D on adolescent bone growth/density we used a novel juvenile genetic model (Ins2+/- mice) that spontaneously develop T1D at approximately 5 weeks of age and compared our findings with STZ-induced T1D mice. Compared to controls, both Ins2+/- and STZ-induced T1D mice displayed blood glucose levels greater than 300mg/dl and reduced body, fat and muscle mass as well as femur trabecular bone density. STZ mice exhibited greater bone loss compared to Ins2+/- mice despite having lower blood glucose levels. Cortical bone was affected in STZ but not Ins2+/- mice. Osteocalcin serum protein and bone RNA levels decreased in both models. Consistent with studies in adult mice, STZ adolescent mice displayed increased marrow adiposity, however this was not observed in the Ins2+/- mice. Reduced femur length, decreased growth plate thickness and decreased collagen II expression in both model simplies impaired cartilage formation. In summary, both pharmacologic and spontaneous adolescent T1D mice demonstrated a bone synthesis and growth defect. STZ appears to cause a more severe phenotype. Thus, the Ins2+/- mouse could serve as a useful model to study adolescent T1D bone loss with fewer complications.
机译：青少年骨骼进行加速增长确定总体骨质密度、长度、和质量。(近年来),在青少年最常诊断,可以改变骨过程,促进骨质流失。研究1型糖尿病(近年来)疾病通常利用成年老鼠和依赖链脲霉素等药理模型(STZ)全身糖尿病啮齿动物。近年来对青少年骨骼生长/密度的影响我们使用了一个新颖的少年(isn2 + / -遗传模型自发发展近年来的老鼠)大约5周的年龄和我们相比发现与STZ-induced内转至老鼠。控制,isn2 + / -和STZ-induced内转至老鼠血糖水平大于显示300 mg / dl,减少身体的脂肪和肌肉以及股骨骨小梁密度。表现出更强的骨质流失而isn2 + / -老鼠虽然降低血糖水平。皮质骨在STZ影响但不是isn2 + / -老鼠。在两模型水平下降。成年小鼠的研究,STZ青少年老鼠然而,显示增加骨髓脂肪过多这不是在isn2 + / -老鼠。降低股骨长度,降低生长板厚度和减少胶原蛋白II表达两个模型简单受损软骨形成。总之,药物和自发的青少年内转至小鼠表现出骨合成和生长缺陷。严重的表型。作为一个有用的模型来研究青少年内转用更少的并发症骨质流失。

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