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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Adverse Effects of Diabetes Mellitus on the Skeleton of Aging Mice
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Adverse Effects of Diabetes Mellitus on the Skeleton of Aging Mice

机译:糖尿病对衰老小鼠骨骼的不利影响

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In the present study, the possibility that a diabetic (DM) status might worsen age-related bone deterioration was explored in mice. Male CD-1 mice aged 2 (young control group) or 16 months, nondiabetic or made diabetic by streptozotocin injections, were used. DM induced a decrease in bone volume, trabecular number, and eroded surface, and in mineral apposition and bone formation rates, but an increased trabecular separation, in L1-L3 vertebrae of aged mice. Three-point bending and reference point indentation tests showed slight changes pointing to increased frailty and brittleness in the mouse tibia of diabetic old mice. DM was related to a decreased expression of both vascular endothelial growth factor and its receptor 2, which paralleled that of femoral vasculature, and increased expression of the pro-adipogenic gene peroxisome proliferator-activated receptor. and adipocyte number, without affecting beta-catenin pathway in old mouse bone. Concomitant DM in old mice failed to affect total glutathione levels or activity of main anti-oxidative stress enzymes, although xanthine oxidase was slightly increased, in the bone marrow, but increased the senescence marker caveolin-1 gene. In conclusion, DM worsens bone alterations of aged mice, related to decreased bone turnover and bone vasculature and increased senescence, independently of the anti-oxidative stress machinery.
机译:在本研究中,在小鼠中探讨了糖尿病(DM)状态可能加剧与年龄有关的骨骼退化的可能性。使用年龄为2岁(年轻对照组)或16个月,无糖尿病或通过链脲佐菌素注射治疗糖尿病的雄性CD-1小鼠。 DM导致衰老小鼠L1-L3椎骨中骨量,小梁数量减少和表面腐蚀以及矿物质沉积和骨形成速率降低,但小梁间距增加。三点弯曲和参考点压痕测试显示,糖尿病老年小鼠的小鼠胫骨中的脆弱和脆性增加,略有变化。 DM与血管内皮生长因子及其受体2的表达降低(与股血管结构的表达平行)和促脂肪基因过氧化物酶体增殖物激活受体的表达增加有关。和脂肪细胞数量,而不会影响老小鼠骨骼中的β-catenin途径。老年小鼠中的DM不能影响总谷胱甘肽水平或主要抗氧化应激酶的活性,尽管黄嘌呤氧化酶在骨髓中略有增加,但增加了衰老标记caveolin-1基因。总之,DM会增加衰老小鼠的骨骼变化,这与骨骼更新和骨骼脉管系统的减少以及衰老的增加有关,而与抗氧化应激机制无关。

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