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首页> 美国卫生研究院文献>Journal of Bone and Mineral Research >Type 1 Diabetes in Young Rats Leads to Progressive Trabecular Bone Loss Cessation of Cortical Bone Growth and Diminished Whole Bone Strength and Fatigue Life
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Type 1 Diabetes in Young Rats Leads to Progressive Trabecular Bone Loss Cessation of Cortical Bone Growth and Diminished Whole Bone Strength and Fatigue Life

机译：幼年大鼠的1型糖尿病会导致渐进性小梁骨丢失皮质骨生长停止以及全骨强度和疲劳寿命降低

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People with diabetes have increased risk of fracture disproportionate to BMD, suggesting reduced material strength (quality). We quantified the skeletal effects of type 1 diabetes in the rat. Fischer 344 and Sprague-Dawley rats (12 wk of age) were injected with either vehicle (Control) or streptozotocin (Diabetic). Forelimbs were scanned at 0, 4, 8, and 12 wk using pQCT. Rats were killed after 12 wk. We observed progressive osteopenia in diabetic rats. Trabecular osteopenia was caused by bone loss: volumetric BMD decreased progressively with time in diabetic rats but was constant in controls. Cortical osteopenia was caused by premature arrest of cortical expansion: cortical area did not increase after 4–8 wk in diabetic rats but continued to increase in controls. Postmortem μCT showed a 60% reduction in proximal tibial trabecular BV/TV in diabetic versus control rats, whereas moments of inertia of the ulnar and femoral diaphysis were reduced ∼30%. Monotonic bending tests indicated that ulna and femora from diabetic animals were ∼25% less stiff and strong versus controls. Estimates of material properties indicated no changes in elastic modulus or ultimate stress but modest (∼10%) declines in yield stress for diabetic bone. These changes were associated with a ∼50% increase in the nonenzymatic collagen cross-link pentosidine. Last, cyclic testing showed diminished fatigue life in diabetic bones at the structural (force) level but not at the material (stress) level. In summary, type 1 diabetes, left untreated, causes trabecular bone loss and a reduction in diaphyseal growth. Diabetic bone has greatly increased nonenzymatic collagen cross-links but only modestly reduced material properties. The loss of whole bone strength under both monotonic and fatigue loading is attributed mainly to reduced bone size.
机译：糖尿病患者发生骨折的风险与BMD不成比例，表明材料强度（质量）降低。我们量化了大鼠1型糖尿病的骨骼作用。给Fischer 344和Sprague-Dawley大鼠（年龄12周龄）注射媒介物（对照）或链脲佐菌素（糖尿病）。使用pQCT在0、4、8和12周扫描前肢。 12周后杀死大鼠。我们在糖尿病大鼠中观察到进行性骨质减少。小梁性骨质减少是由骨质流失引起的：在糖尿病大鼠中，BMD随时间逐渐减少，而在对照组中则保持恒定。皮质骨质减少症是由皮质扩张的过早停止引起的：糖尿病大鼠在4-8周后皮质面积并未增加，但在对照组中继续增加。死后μCT显示，与对照组相比，糖尿病大鼠胫骨小梁近端BV / TV降低了60％，而尺骨和股骨干的惯性矩降低了约30％。单调弯曲试验表明，与对照组相比，糖尿病动物的尺骨和股骨硬度降低了约25％。材料性能的估计表明，糖尿病骨的弹性模量或极限应力没有变化，但屈服应力却有适度下降（约10％）。这些变化与非酶胶原交联戊糖苷的增加约50％有关。最后，循环测试显示糖尿病骨骼的疲劳寿命在结构（受力）水平上降低了，但在物质（应力）水平上没有降低。总之，未经治疗的1型糖尿病会导致小梁骨丢失和干骨生长减少。糖尿病骨极大地增加了非酶胶原交联，但仅适度降低了材料性能。在单调负荷和疲劳负荷下全骨强度的损失主要归因于骨尺寸的减小。

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