IN VIVO STUDIES OF ETHANOL AGING AND OSTEOPENIA

长期摄入酒精是骨质疏松症的主要风险因素， 尤其是在男人身上。骨质疏松症反过来又是一个重要的危险因素 一系列骨折，即髋部、椎骨、Colles‘s骨折及其伴随的 死亡率和发病率。酒精对人体的影响是有据可查的。 以及动物研究，特别是啮齿动物。啮齿动物对骨骼疾病的研究， 然而，在成人条件下的应用有限，因为 大多数啮齿类动物的骨痂一直保持开放，直到它们死亡。中国人的骨代谢 有开放骨痂的动物被认为与 骨痂闭合的动物。此应用程序试图检查 慢性酒精摄入对特异性骨代谢的影响 衰老大鼠品系(Fisher 344)。这种动物已经记录在案 大约15个月龄时骨痂闭合。此外，其他 矿物质代谢参数，例如钙吸收，密切相关 模仿那些在上了年纪的人身上看到的。因此，乙醇在这方面的成功使用 骨量减少的模型将把这一系统建立为 研究酒精所致人体骨量丢失的合适模型。 最初的研究将检验不同数量的乙醇的影响。 老年(21月龄)雄性F344大鼠的骨量变化。已经确立了 最佳膳食酒精水平，长期研究的效果 乙醇对矿物质代谢参数的影响将被承担。血清 尿中的磷酸钙，肌酐，镁的水平将是 下定决心。骨量和矿物质将用 骨生物学的非脱钙组织形态计量学研究 成骨细胞和破骨细胞特异性染色。血清促钙素水平 激素，甲状旁腺激素，25羟基和1，25二羟基维生素D 将进行级别测试。 第二年将审查旨在实现以下目标的战略(主要是饮食) 使用乙醇减少或消除该模型中出现的骨丢失 摄取。上述矿物质代谢参数将为 在适当的时候遵循。 这些研究应该允许建立雄性Fisher 344大鼠 作为研究与酒精有关的骨丢失的合适模型，以及 提供矿物质干扰的初步迹象 新陈代谢发生了，如果有任何饮食控制可能会改变他们。

Chronic ethanol ingestion is a major risk factor for osteoporosis, particularly in men. Osteoporosis in turn is a significant risk factor for a series of fractures, i.e. hip, vertebrae, Colles', with their attendant mortality and morbidity. The effect of ethanol is well documented in man and animal studies, particularly rodents. Rodent studies of bone disease, however, have limited application to adult human conditions because the epiphyses of most rodents remain-open until they die. Bone metabolism in animals with open epiphyses is thought to be much different than that in animals with closed epiphyses. This application seeks to examine the effect of chronic ethanol ingestion on the bone metabolism of a specific strain of aging rat (Fisher 344). This type of animal has documented closure of epiphyses at about fifteen months of age. In addition, other parameters of mineral metabolism, for example, calcium absorption, closely mimic those seen in aging man. Thus, the successful use of ethanol in this model with reduction in bone mass would establish this system as an appropriate model to study ethanol related loss of bone mass in man. The initial studies will examine the effect of varying amounts of ethanol on bone mass in elderly (21 month old) male F344 rats. Having established an optimal dietary ethanol level, long term studies of the effect of ethanol on the parameters of mineral metabolism will be undertaken. Serum and urine levels of calcium phosphate, creatinine, magnesium will be determined. Bone weight and mineral will be determined with non-decalcified histomorphometry studies of bone biology as well as osteoblast and osteoclast specific stains. Serum levels of calciotropic hormones, parathyroid hormone, 25 hydroxy and 1,25 dihydroxy vitamin D levels will be performed. The second year will examine strategies (primarily dietary) aimed at reducing or eliminating the bone loss seen in this model with ethanol ingestion. Parameters of mineral metabolism described above will be followed when appropriate. These studies should allow the establishment of the male Fisher 344 rats as an appropriate model to study alcohol related bone loss, as well as provide a preliminary indication of what if any disturbances in mineral metabolism occur and what if any dietary manipulations may alter them.