Although postmenopausal osteoporosis often occurs concurrently with diabetes, little is known about interactions between estrogen deficiency and hyperglycemia in the skeletal system. In the present study, the effects of estrogen deficiency on the development of biochemical, microstructural, and mechanical changes induced by streptozotocin-induced diabetes mellitus (DM) in the rat skeletal system were investigated. The experiments were carried out on nonovariectomized (NOVX) and ovariectomized (OVX) control and diabetic mature female Wistar rats. Serum levels of bone turnover markers (CTX-I and osteocalcin) and 23 cytokines, bone mass and mineralization, histomorphometric parameters, and mechanical properties of cancellous and compact bone were determined. The results were subjected to two-way ANOVA and principal component analysis (PCA). Estrogen deficiency induced osteoporotic changes, with increased bone resorption and formation, and worsening of microstructure (femoral metaphyseal BV/TV decreased by 13.0%) and mechanical properties of cancellous bone (the maximum load in the proximal tibial metaphysis decreased by 34.2%). DM in both the NOVX and OVX rats decreased bone mass, increased bone resorption and decreased bone formation, and worsened cancellous bone microarchitecture (for example, the femoral metaphyseal BV/TV decreased by 17.3% and 18.1%, respectively, in relation to the NOVX controls) and strength (the maximum load in the proximal tibial metaphysis decreased by 35.4% and 48.1%, respectively, in relation to the NOVX controls). Only in the diabetic rats, profound increases in some cytokine levels were noted. In conclusion, the changes induced by DM in female rats were only slightly intensified by estrogen deficiency. Despite similar effects on bone microstructure and strength, the influence of DM on the skeletal system was based on more profound systemic homeostasis changes than those induced by estrogen deficiency.

中文翻译：

---

在实验大鼠模型中，雌激素缺乏对 1 型糖尿病引起的骨骼变化发展的影响可以忽略不计

尽管绝经后骨质疏松症通常与糖尿病同时发生，但对雌激素缺乏与骨骼系统高血糖之间的相互作用知之甚少。在本研究中，研究了雌激素缺乏对链脲佐菌素诱导的糖尿病 (DM) 大鼠骨骼系统生化、微观结构和机械变化发展的影响。实验是在非去卵巢 (NOVX) 和去卵巢 (OVX) 对照和糖尿病成熟雌性 Wistar 大鼠上进行的。测定了骨转换标志物（CTX-I 和骨钙素）和 23 种细胞因子的血清水平、骨量和矿化、组织形态学参数以及松质骨和致密骨的机械特性。结果进行了双向方差分析和主成分分析（PCA）。雌激素缺乏引起骨质疏松改变，骨吸收和形成增加，微观结构恶化（股骨干骺端 BV/TV 下降 13.0%）和松质骨力学性能（胫骨近端干骺端的最大负荷下降 34.2%）。NOVX 和 OVX 大鼠的 DM 减少骨量，增加骨吸收和减少骨形成，并恶化松质骨微结构（例如，与 NOVX 相比，股骨干骺端 BV/TV 分别降低了 17.3% 和 18.1%控制）和强度（与 NOVX 控制相比，胫骨近端干骺端的最大负荷分别降低了 35.4% 和 48.1%）。仅在糖尿病大鼠中，注意到某些细胞因子水平显着增加。综上所述，雌性大鼠 DM 引起的变化仅因雌激素缺乏而略微加剧。尽管对骨骼微观结构和强度的影响相似，但 DM 对骨骼系统的影响是基于比雌激素缺乏引起的更深刻的全身稳态变化。