Hough F S
S Afr Med J. 1987 Jul 18;72(2):116-9.
A critical review of the literature leads to the conclusion that alterations of bone and mineral metabolism occur both in diabetic patients and in animals with experimentally induced insulin deficiency syndromes. The coexistence of juvenile insulin-dependent diabetes mellitus (type 1) and radiological evidence of decreased bone mass (osteopenia) appears to be firmly established. Available data support the view that these patients have an increased propensity to skeletal fracture. Adult-onset, non-insulin-dependent diabetic populations, more heterogeneous as regards the type of diabetes, the therapy and the presence of complications or coexistent disease, are characterised by subpopulations with either a decreased, a normal or an increased bone mass. The pathogenesis of diabetic osteopenia is multifactorial. Data obtained from studies employing appropriate animal models of chronic insulin deficiency indicate that various metabolic and hormonal abnormalities may be involved.
对文献的批判性综述得出结论，骨和矿物质代谢的改变在糖尿病患者以及实验性诱导胰岛素缺乏综合征的动物中均会发生。青少年胰岛素依赖型糖尿病（1型）与骨量减少（骨质减少）的放射学证据并存这一现象似乎已确凿无疑。现有数据支持这样的观点，即这些患者发生骨骼骨折的倾向增加。成年发病的非胰岛素依赖型糖尿病群体，在糖尿病类型、治疗方法以及并发症或并存疾病的存在方面更为多样化，其特征是存在骨量减少、正常或增加的亚群体。糖尿病性骨质减少的发病机制是多因素的。从使用慢性胰岛素缺乏的适当动物模型进行的研究中获得的数据表明，可能涉及各种代谢和激素异常。
