The association between the baseline bone resorption marker CTX and incident dysglycemia after 4 years.
The association between the baseline bone resorption marker CTX and incident dysglycemia after 4 years.
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基线骨吸收标志物 CTX 与 4 年后发生血糖异常之间的关联
DOI：
10.1038/boneres.2017.20
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发表时间：
2017
期刊：
影响因子：
12.7
通讯作者：
Tao B
中科院分区：
文献类型：
--
作者：
Liu TT;Liu DM;Xuan Y;Zhao L;Sun LH;Zhao DD;Wang XF;He Y;Guo XZ;Du R;Wang JQ;Liu JM;Zhao HY;Tao B
骨骼是参与调节血糖动态平衡的内分泌器官。骨形成标记物骨钙素(OCN)在预测糖尿病中的作用已有报道，但结果相互矛盾。还没有研究探讨基线骨吸收活动与糖尿病或糖尿病前期事件在随访期间的关系。我们的目的是研究基础骨吸收标记物交联型I型胶原C-端肽(CTX)与4年后血糖紊乱的关系。这项纵向研究是在一所大学教学医院进行的。共有195名基线水平的正常糖耐量(NGT)女性被邀请进行随访。记录糖尿病和糖尿病前期(统称为血糖异常)的发生率。共有128人完成了这项为期4年的研究。从NGT到血糖异常的总转化率为31.3%。血糖异常发生率以环磷酰胺中段最低[16.3%(95%可信区间，6.8%~30.7%)]，低于环磷酰胺下段[31.0%(95%可信区间，17.2%~46.1%)]和上段[46.5%(95%可信区间，31.2%~62.6%)]，差异有统计学意义(P=0.002 5)。在调整了多个混杂变量后，基线CTX的上三分位数与发生血糖异常的风险增加相关，当以中三分位数为参考时，优势比为7.09(95%CI，1.73-28.99)。在一个双相模型中，破骨细胞主动调节葡萄糖稳态，在基线水平适度增强的骨吸收标记物CTX提供保护作用，防止葡萄糖代谢的恶化，而过度活跃的破骨细胞功能有助于增加后续血糖紊乱的风险。
Bone is an endocrine organ involved in modulating glucose homeostasis. The role of the bone formation marker osteocalcin (OCN) in predicting diabetes was reported, but with conflicting results. No study has explored the association between baseline bone resorption activity and incident diabetes or prediabetes during follow-up. Our objective was to examine the relationship between the baseline bone resorption marker crosslinked C-telopeptide of type I collagen (CTX) and glycemic dysregulation after 4 years. This longitudinal study was conducted in a university teaching hospital. A total of 195 normal glucose tolerant (NGT) women at baseline were invited for follow-up. The incidence of diabetes and prediabetes (collectively defined as dysglycemia) was recorded. A total of 128 individuals completed the 4-year study. The overall conversion rate from NGT to dysglycemia was 31.3%. The incidence of dysglycemia was lowest in the middle tertile [16.3%(95% confidence interval (CI), 6.8%–30.7%)] compared with the lower [31.0%(95% CI, 17.2%–46.1%)] and upper [46.5%(95% CI, 31.2%–62.6%)] tertiles of CTX, with a significant difference seen between the middle and upper tertiles (P= 0.002 5). After adjusting for multiple confounding variables, the upper tertile of baseline CTX was associated with an increased risk of incident dysglycemia, with an odds ratio of 7.09 (95% CI, 1.73–28.99) when the middle tertile was the reference. Osteoclasts actively regulate glucose homeostasis in a biphasic model that moderately enhanced bone resorption marker CTX at baseline provides protective effects against the deterioration of glucose metabolism, whereas an overactive osteoclastic function contributes to an increased risk of subsequent dysglycemia.