TWIN AND FAMILY STUDIES OF BONE MASS

双胞胎和家庭的骨量研究

• 批准号: 3745823
• 负责人: JOE C CHRISTIAN
• 金额: --
• 依托单位: INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3745823
• 关键词: DNA; aging; alcoholic beverage consumption; automated data processing; biomarker; blood; blood chemistry; body weight; bone density; bone development; bone fracture; bone metabolism; caffeine; dietary calcium; dizygotic twins; exercise; family genetics; femur; gene mutation; human subject; hypercholesterolemia; interview; linkage mapping; longitudinal human study; molecular genetics; monozygotic twins; nutrition related tag; osteoporosis; phenotype; photon absorptiometry; questionnaires; siblings; southern blotting; spine; tobacco abuse

The primary objective of this project is to define genetic an environmental contributions to the development and maintenance of peak bone mass in healthy, free-living subjects. Primary osteoporosis is a long term disease characterized by increased susceptibility to fractures and low bone mass at the fracture site. Its effects are felt by 20 million elderly individuals in this country, a figure that will increase as our population ages and may also be increasing due to changing lifestyles. Genetic studies are difficult because osteoporotic fractures happen so late in life. We have therefore concentrated on the study of bone mass as a risk factor for osteoporosis. Bone mass in the elderly is a function of peak bone mass and subsequent loss that starts as early as the fourth decade of life. There i a great deal of individual variation in peak bone mass and a number of family and twin studies have found that half or more of this variance is genetic. Therefore, development of peak bone mass is undoubtedly under som degree of genetic control. However, longitudinal data to estimate and characterize the influence of genetic factors on bone mass development are not available. In our study of 171 pairs of adult female twins we found evidence suggestive of the interactions of a relatively few major genes tha influence adult bone mass. There is a great deal of variation in rate of bone loss with aging, but little is known about genetic influences on this second factor contributing to osteoporosis. In the only longitudinal genetic study of bone mass loss with aging we found familial relationships in aging twins but no evidence for genetic influences. However, this study was limited to males and the radius which does not bear weight and is 90% cortical bone. We propose to continue twin studies, started up to 20 years ago, to estimat genetic and environmental influences on bone mass and extend these studies to measure genetic influences on rate of bone development and rate of loss. In addition, we will ascertain families with extreme values of bone mass in a search for evidence of segregating genes.

该项目的主要目的是定义遗传环境 对峰值骨质的发展和维持的贡献 健康，自由生活的主题。 原发性骨质疏松症是长期疾病 其特征是在 断裂部位。 2000万年长的人感觉到它的影响 在这个国家，随着我们人口的年龄的增长，这个数字可能会增加 由于生活方式的改变，也会增加。 遗传研究是 很难，因为骨质疏松性骨折是如此晚期发生。 我们有 因此，集中于骨骼质量的研究 骨质疏松症。 老年人中的骨骼质量是峰骨质的函数， 随后的损失早在生命的第四个十年开始。 那里我 峰骨质量和许多个人变化很大 家庭和双胞胎研究发现，这种差异的一半是 遗传。 因此，峰值骨质的发展无疑是在SOM下的 遗传控制程度。 但是，纵向数据要估计和 表征遗传因素对骨骼质量发育的影响是 无法使用。 在我们对171对成年女双胞胎的研究中，我们发现 证明相对较少的主要基因相互作用的证据 影响成人骨骼。 速率有很大差异 随着衰老的骨质流失，但对此对遗传影响知之甚少 导致骨质疏松症的第二个因素。 在唯一的纵向 与衰老的骨骼质量损失的遗传研究我们发现家族关系 在衰老的双胞胎中，但没有证据表明遗传影响。 但是，这项研究 仅限于男性，半径不承受重量，为90％ 皮质骨。 我们建议继续进行双胞胎研究，始于20年前，以估计 遗传和环境对骨骼质量的影响并扩展这些研究 衡量遗传对骨骼发育速率和损失率的影响。 此外，我们将确定具有极端骨骼质量值的家庭 寻找分离基因的证据。