SKELETAL EFFECTS OF LEPTIN IN ADULT ESTROGEN DEPLETION

体重是骨量的主要决定因素。这种影响并不是 通过任一力学假设（载荷增加）充分解释 或与脂肪增加相关的雌激素水平升高， 身体质量和骨质之间的其他联系。瘦素， 发现的脂肪来源的饱腹感激素，可能构成了寻求的- 脂肪量和骨质之间的联系。 Matkovic等人（1997年a和B） 已经表明瘦素可能对骨膜骨具有合成代谢作用， 阵此外，Liu等人（1997）已经表明，给予 ob/ob小鼠产生皮质内骨形成的显著增加。在 目前，还没有关于瘦素与骨相互作用的其他研究。 我们建议检查瘦素和骨之间的相互关系 使用成年大鼠作为模型。我们将检验这个假设， 骨对瘦素的反应1）是合成代谢的，并导致骨增加， 质量和强度，2）具有剂量依赖性，3）发生在松质骨和 皮质骨，4）影响骨膜和骨内膜表面，以及5） 与雌激素状态无关。密度测定，生物力学，和 将评估组织形态学反应。

Body mass is a major determinant of bone mass. This effect is not adequately explained by either mechanical hypothesis (increased loading) or the higher estrogen status associated with increased fat, suggesting some other link between body mass and bone mass. Leptin, the newly discovered adiposite- derived satiety hormone, may constitute the sought- for link between fat mass and bone mass. Matkovic et al. (1997a and b) have shown that leptin may have an anabolic effect on periosteal bone formation. Furthermore, Liu et al. (1997) have shown that leptin given to ob/ob mice produces a dramatic increase in endocortical bone formation. At the present time, no other work has been done on leptin bone interactions. We propose to examine the inter-relationship between leptin and bone formation using the adult rat as a model. We will test the hypothesis that bone response to leptin 1) is anabolic and results in an increase in bone mass and strength, 2) is dose dependent, 3) occurs in both cancellous and cortical bone, 4) effects the periosteal and endosteal surfaces, and 5) is independent of estrogen status. Densitometric, biomechanical, and histomorphometric response will be assessed.