老年性骨质疏松症：一种年龄相关的脂代谢障碍疾病  

Senile osteoporosis： age-related disease of lipid metabolism

作　　者：张雪竹[1] 彭应梅[1] 于建春[1] 韩景献[1] 

机构地区：[1]天津中医药大学第一附属医院针灸研究所,300193

出　　处：《国际内分泌代谢杂志》2007年第5期348-351,共4页International Journal of Endocrinology and Metabolism

基　　金：国家自然科学基金重点项目（30630074）;天津市应用基础及前沿技术研究计划重点项目（07JCZDJC08800）;教育部高等学校博士学科点专项科研基金（20060063006）;天津市卫生局资助课题（2005034）

摘　　要：随着年龄的增加,骨髓中脂细胞逐渐增多,成骨细胞数量及成骨活性下降,破骨活跃,最终导致骨质疏松,但这种病理改变的机制仍不清楚。近来发现可能与以下因素有关：骨髓微环境发生变化;前脂细胞老化导致细胞因子生成增多,影响其脂肪酸代谢方式和对胰岛素的敏感性;过氧化物酶体增殖物活化受体（PPAR）γ等转录因子表达随年龄下降,导致脂细胞分化相关基因表达减少,成脂功能障碍;骨髓间充质干细胞分化方向发生改变,最终造成脂库储脂能力降低及脂质的异位积聚。With aging,the composition of bone marrow shifts to favor the presence of adipocytes,the increase of osteoclast activity,and the decrease of osteoblast function resulting in osteoporosis. The mechanisms underlying these age-related pathogenic changes are not clearly understood ,perhaps due to the change of bone marrow microenvironment,altered fatty acid handling and impaired insulin sensitivity resulted from increased preadipocyte eytokine generation with aging, decreased abundance of peroxisome proliferator activated receptor （PPAR）γresulting in impaired adipogenesis and reduced expression of differentiation dependent genes in fat cells, and dysdifferentiation of mesenchymal stem cells （MSC）. This, in turn, contributes to fat cell dysfunction, reduced fat depot size ,and redistribution of fat to muscle ,bone marrow ,and other tissues,

关 键 词：老年性骨质疏松症 脂质代谢 细胞分化 骨髓 间充质干细胞 

分 类 号：R5[医药卫生—内科学]