NUTRITIONAL REGULATION OF BONE TURNOVER

骨质疏松症影响着大约2800万美国人，是一种主要的疾病。 老年男女的死亡原因。据估计，在 女性（50岁以上），高达50%的骨质减少（低骨量）和18%的 骨质疏松骨质疏松症的风险增加的妇女体重低， 那些有减肥史的人。此外，PI显示， 适度的体重减轻导致肥胖妇女的骨动员和损失。 此外，对非自愿体重减轻的研究表明， 瘦的女性比胖的女性损失更大。这些研究将 说明超重（体重）患者的骨动员和骨丢失是否更大 指数，BMI 25 - 29.9）比肥胖（BMI> 30）绝经前后 女性在中度自愿体重减轻期间。我们的数据显示， 血清甲状旁腺激素（PTH）和性激素减少可能是 调节骨转换的上升和体重减轻。据推测， 热量限制期间钙吸收减少是导致 PTH升高。我们建议研究营业额和PTH上升的基础 在热量限制期间，通过检查总钙吸收分数 在重量损失期间。在肥胖女性中，PI发现1.6 mg/d的钙可以抑制 与重量损失相关的骨移动和损失。但不 已知这种水平的钙摄入量是否可以抑制"稀释剂"中的骨动员 在热量限制期间超重的女性。此外，有可能 目前推荐的摄入量水平（1 - 1.2 g/d）在体重减轻期间是不够的 基于其他人对wt损失引起的骨损失的研究。因此这些 研究将检查在2 ℃时热量限制期间的骨转换和质量 钙摄入水平（足够或高），以确定体重减轻的最佳水平。 重要的是，对大鼠的研究表明， 限制（尽管有足够的钙摄入量）。为了了解骨骼的质量 随着体重减轻而改变，无论它是否依赖于初始体重，我们 将检查慢性热疗后骨骼的超微结构特性， 限制肥胖和瘦大鼠。这些研究的长期目标是 确定营养对骨骼的影响， 和骨质疏松症的治疗。

Osteoporosis affects approximately 28 million Americans, and is a leading cause of death among older men and women. It has been estimated that in women (50+ years), up to 50% have osteopenia (low bone mass) and 18% have osteoporosis. The risk of osteoporosis increases in women of low body weight or those who have a history of weight loss. In addition, the PIs have shown that moderate weight loss results in bone mobilization and loss in obese women. Moreover, studies of involuntary wt loss show that the magnitude of the bone loss is greater in thinner than heavier women. Hence, these studies will address whether bone mobilization and loss is greater in overweight (body mass index, BMI 25-29.9) than obese (BMI more than 30 ) pre- and post menopausal women during moderate voluntary wt loss. Our data show that an increase in serum parathyroid hormone (PTH) and a decrease in sex hormones may be regulating the rise in bone turnover with wt loss. It is hypothesized that a reduced calcium absorption during caloric restriction is responsible for the rise in PTH. We propose to study the basis for the rise in turnover and PTH during caloric restriction by examining total fractional calcium absorption during wt loss. In obese women, the PIs found that 1.6 mg/d of Ca can suppress the bone mobilization and loss associated with wt loss. However, it is not known if this level of Ca intake can suppress bone mobilization in "thinner" overweight women during caloric restriction. Also, it is possible that the current recommended level of intake (1-1.2 g/d) is not adequate during wt loss based on studies of wt loss induced bone loss by others. Therefore, these studies will examine bone turnover and mass during caloric restriction at 2 levels of Ca intake (adequate or high) to determine optimal levels for wt loss. Importantly, rat studies show that fracture risk is increased with caloric restriction (despite adequate Ca intake). To understand how the quality of bone is altered with wt loss, and whether it is dependent on initial body wt, we will examine the ultrastructural properties of bone after chronic caloric restriction in obese and lean rats. Long-term goals of these studies are to determine nutritional influences on bone which can be applied in the prevention and treatment of osteoporosis.