期刊
JOURNAL OF BONE AND MINERAL RESEARCH
卷 26, 期 1, 页码 79-87出版社
WILEY
DOI: 10.1002/jbmr.192
关键词
BONE MINERAL DENSITY; FAT MASS; LEAN MASS; TWIN STUDIES; GENETIC CORRELATION
资金
- National Institute on Alcohol Abuse and Alcoholism [AA-08315, AA-00145, AA-12502]
- European Union [QLRT-1999-00916, QLG2-CT-2002-01254]
- DiOGenes Project
- Academy of Finland [44069, 100499, 201461]
- Academy of Finland Centre of Excellence in Complex Disease Genetics
- Helsinki University Central Hospital
- Yrjo Jahnsson
- Juho Vainio
- Jalmari and Rauha Ahokas
- Biomedicum Helsinki
- Research Foundation of the University of Helsinki
- Novo Nordisk Foundations
- European Community [FOOD-CT-2005-513946]
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R37AA012502, R01AA012502, R01AA008315, K05AA000145] Funding Source: NIH RePORTER
The purpose of this study was to investigate the relationship of fat mass (FM) and lean mass (LM) with bone mineral density (BMD) independent of genetic effects. We also assessed the extent to which genetic and environmental influences explain the associations between these phenotypes. Body composition and BMD were measured using dual-energy X-ray absorptiometry in 57 monozygotic and 92 same-sex dizygotic twin pairs, aged 23 to 31 years, chosen to represent a wide range of intrapair differences in body mass index (BMI; 0 to 15.2 kg/m(2)). Heritability estimates were adjusted for height and gender. In multiple linear regression analysis, intrapair differences in both FM and LM were independently associated with intrapair differences in BMD at most skeletal sites after adjustment for gender and differences in height. Within monozygotic and dizygotic pairs, LM was a significantly stronger predictor of whole-body BMD than FM (p<.01). Additive genetic factors explained 87% [95% confidence interval (Cl) 80%-91%), 81% (95% Cl 70%-88%), and 61% (95% Cl 41%-75%) of the variation in whole-body BMD, LM, and FM, respectively. Additive genetic factors also accounted for 69% to 88% of the covariance between LM and BMD and for 42% to 72% of the covariance between FM and BMD depending on the skeletal site. The genetic correlation between LM and whole-body BMD (r(g)=0.46, 95% Cl 0.32-0.58) was greater than that of FM and whole-body BMD (r(g)=0.25, 95% Cl 0.05-0.42). In conclusion, our data indicate that peak BMD is influenced by acquired body weight as well as genetic factors. In young adulthood, LM and BMD may have more genes in common than do FM and BMD. (C) 2011 American Society for Bone and Mineral Research.
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