Type 2 diabetes and bone fragility in children and adults.

Type 2 diabetes and bone fragility in children and adults.
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DOI:
10.4239/wjd.v13.i11.900
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发表时间:
2022-11-15
影响因子:
4.2
通讯作者:
Brunetti G
Brunetti G
中科院分区:
医学3区
文献类型:
--
作者:
Faienza MF;Pontrelli P;Brunetti G

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2型糖尿病(T2 D)是一种全球性流行病。T2 D在青少年和年轻人中的患病率正在惊人地增加。导致年轻人T2 D的机制与老年患者相似。然而,发病的严重程度、胰岛素敏感性降低和胰岛素分泌缺陷在较年轻时发生疾病的受试者中可能不同。T2 D与不同的并发症相关,包括骨脆性,从而易发生骨折。本系统综述的目的是描述T2 D骨脆性以及所有可能涉及的途径。许多研究报告称,与对照组相比,T2 D患者的骨矿物质密度保持不变,甚至增加。这种明显的矛盾可以通过骨质量的改变和皮质骨孔隙率的增加以及机械性能的改善来解释。此外,在T2 D中描述了骨转换减少,骨形成和吸收标志物减少。这些发现促使不同的研究人员强调导致骨脆性的机制,并且已经确定和研究了许多关键的改变途径。具体而言,我们将注意力集中在微血管疾病、晚期糖基化终末产物、衰老通路、Wnt/β-连环蛋白通路、骨保护素/核因子κ B受体激活剂配体、骨连接素和成纤维细胞生长因子23的作用。对2型骨髓性骨脆性的理解是一个重要问题,因为它可以提示可能的干预措施,以预防T2 D中的骨质不良和/或如何在骨病明显时靶向这些途径。
Type 2 diabetes (T2D) is a global epidemic disease. The prevalence of T2D in adolescents and young adults is increasing alarmingly. The mechanisms leading to T2D in young people are similar to those in older patients. However, the severity of onset, reduced insulin sensitivity and defective insulin secretion can be different in subjects who develop the disease at a younger age. T2D is associated with different complications, including bone fragility with consequent susceptibility to fractures. The purpose of this systematic review was to describe T2D bone fragility together with all the possible involved pathways. Numerous studies have reported that patients with T2D show preserved, or even increased, bone mineral density compared with controls. This apparent paradox can be explained by the altered bone quality with increased cortical bone porosity and compr-omised mechanical properties. Furthermore, reduced bone turnover has been described in T2D with reduced markers of bone formation and resorption. These findings prompted different researchers to highlight the mechanisms leading to bone fragility, and numerous critical altered pathways have been identified and studied. In detail, we focused our attention on the role of microvascular disease, advanced glycation end products, the senescence pathway, the Wnt/β-catenin pathway, the osteoprotegerin/receptor-activator of nuclear factor kappa B ligand, osteonectin and fibroblast growth factor 23. The understanding of type 2 myeloid bone fragility is an important issue as it could suggest possible interventions for the prevention of poor bone quality in T2D and/or how to target these pathways when bone disease is clearly evident.
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