Lack of association between interleukin-1 receptor antagonist protein gene polymorphism and bone mineral density in Hungarian postmenopausal women

被引:23
作者
Bajnok, É [1 ]
Takács, I [1 ]
Vargha, P [1 ]
Speer, G [1 ]
Nagy, Z [1 ]
Lakatos, P [1 ]
机构
[1] Semmelweis Univ, Dept Med, H-1083 Budapest, Hungary
关键词
interleukin-1 receptor antagonist protein (IL-1RN); polymorphism; bone mineral density (BMD); osteoporosis;
D O I
10.1016/S8756-3282(00)00360-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The major determinant for risk of osteoporosis in later life is bone mineral density (BMD) attained during early adulthood. Bone mineral density is a complex trait that is presumably influenced by multiple genes. Interleukin-1 receptor antagonist protein (IL-1RN) is an attractive candidate gene for osteoporosis susceptibility, because IL-1RN completely inhibits the stimulatory effects of interleukin-1 (IL-1) on bone resorption in organ cultures and has been implicated in the pathogenesis of osteoporosis. In addition, the IL-1RN gene contains a variable-number tandem repeat polymorphism (VNTR) in intron 2 with three potential protein-binding sites. Recently, an association has been found between this polymorphism and postmenopausal bone loss in the spine. In this study, we use the previously described IL-1RN polymorphism to test for an association between this polymorphism and bone mineral density in our population of postmenopausal women. There was no correlation between alleles or genotypes and BMD in the 286 subjects. Dividing subjects into osteoporotic and healthy groups (osteoporotics and controls), we found no difference in the distribution of alleles or genotypes between groups. We found no association between IL-1RN alleles or genotypes and BMD either at the lumbar spine or the femoral neck within groups. Our data do not support the hypothesis that this IL-1RN gene VNTR polymorphism has an impact on bone mass in postmenopausal women. (Bone 27:559-662; 2000) (C) 2000 by Elsevier Science Inc. All rights reserved.
引用
收藏
页码:559 / 562
页数:4
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