Different effects on bone strength and cell differentiation in pre pubertal caloric restriction versus hypothalamic suppression.
Different effects on bone strength and cell differentiation in pre pubertal caloric restriction versus hypothalamic suppression.
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DOI：
10.1016/j.bone.2011.07.019
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发表时间：
2011-10
期刊：
影响因子：
4.1
通讯作者：
Yingling, V. R.
中科院分区：
文献类型：
--
作者：
Joshi, R. N.;Safadi, F. F.;Barbe, M. F.;Del Carpio-Cano, Fe;Popoff, S. N.;Yingling, V. R.
青春期下丘脑闭经和能量限制影响峰值骨量增加。一种假说认为，能量限制改变了下丘脑功能，导致雌二醇水平受到抑制，从而导致骨质流失。然而，关于能量限制和骨强度的正面和负面结果都有报道。因此，本研究的目的是探讨能量限制和下丘脑抑制在青春期开始对骨机械强度和骨髓来源的细胞的成骨能力在两个模型：雌性大鼠与促性腺激素释放激素拮抗剂（GnRH-α）或30%的能量限制。将23日龄的雌性Sprague道利大鼠分为对照组（C组，n=10）、GnRH-a组（n=10）和能量限制（ER组，n=12）。GnRH-a动物每天接受注射，持续27天。ER组动物接受对照动物摄入量的70%。处死后（50日龄），测量体重、子宫和肌肉重量。培养骨髓基质细胞并测定其增殖和向成骨细胞分化。结果指标包括骨强度、骨组织形态计量学和骨结构、血清IGF-1和骨钙素。与对照组相比，GnRH-a抑制子宫重量，降低成骨细胞增殖、骨强度、骨小梁体积和结构。与GnRH-a组相比，ER模型具有成骨细胞增殖的增加，与对照组相比，相对于体重的骨强度相似，腰椎中的骨小梁体积增加。ER动物较小，但已发育出足以适应其体型的骨强度。相反，通过下丘脑抑制抑制雌二醇导致骨强度缺陷和骨小梁体积损失。总之，我们的研究结果支持这一假设，即在营养应激期间，椎骨体积的增加可能是一种自适应机制，以存储矿物质，这与下丘脑抑制导致的雌二醇抑制不同。
Hypothalamic amenorrhea and energy restriction during puberty affect peak bone mass accrual. One hypothesis suggests energy restriction alters hypothalamic function resulting in suppressed estradiol levels leading to bone loss. However, both positive and negative results have been reported regarding energy restriction and bone strength. Therefore, the purpose of this study was to investigate energy restriction and hypothalamic suppression during pubertal onset on bone mechanical strength and the osteogenic capacity of bone marrow-derived cells in two models: female rats treated with gonadotropin releasing hormone antagonists (GnRH-a) or 30% energy restriction. At 23 days of age, female Sprague Dawley rats were assigned to three groups: control group (C, n=10), GnRH-a group (n=10), and Energy Restriction (ER, n=12) group. GnRH-a animals received daily injections for 27 days. The animals in the ER group received 70% of the control animals’ intake. After sacrifice (50 days of age), body weight, uterine and muscle weights were measured. Bone marrow-derived stromal cells were cultured and assayed for proliferation and differentiation into osteoblasts. Outcome measures included bone strength, bone histomorphometry and architecture, serum IGF-1 and osteocalcin. GnRH-a suppressed uterine weight, decreased osteoblast proliferation, bone strength, trabecular bone volume and architecture compared to control. Elevated serum IGF-1 and osteocalcin levels and body weight were found. The ER model had an increase in osteoblast proliferation compared to the GnRH-a group, similar bone strength relative to body weight and increased trabecular bone volume in the lumbar spine compared to control. The ER animals were smaller but had developed bone strength sufficient for their size. In contrast, suppressed estradiol via hypothalamic suppression resulted in bone strength deficits and trabecular bone volume loss. In summary, our results support the hypothesis that during periods of nutritional stress the increased vertebral bone volume may be an adaptive mechanism to store mineral which differs from suppressed estradiol resulting from hypothalamic suppression.
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影响因子：
3.6
作者：
Engelbregt, MJT;van Weissenbruch, MM;Delemarre-van de Waal, HA
通讯作者：
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影响因子：
5.6
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