Kim Kyong-Chol, Chun Hyejin, Lai ChaoQiang, Parnell Laurence D, Jang Yangsoo, Lee Jongho, Ordovas Jose M
Department of Family Medicine, Chaum Hospital, Cha University, Seoul, Korea,
J Bone Miner Metab. 2015 Mar;33(2):173-9. doi: 10.1007/s00774-014-0570-1. Epub 2014 Feb 26.
Contrary to the traditional belief that obesity acts as a protective factor for bone, recent epidemiologic studies have shown that body fat might be a risk factor for osteoporosis and bone fracture. Accordingly, we evaluated the association between the phenotypes of osteoporosis or vertebral fracture and variants of obesity-related genes, peroxisome proliferator-activated receptor-gamma (PPARG), runt-related transcription factor 2 (RUNX2), leptin receptor (LEPR), and adiponectin (ADIPOQ). In total, 907 postmenopausal healthy women, aged 60-79 years, were included in this study. BMD and biomarkers of bone health and adiposity were measured. We genotyped for four single nucleotide polymorphisms (SNPs) from four genes (PPARG, RUNX2, LEPR, ADIPOQ). A general linear model for continuous dependent variables and a logistic regression model for categorical dependent variables were used to analyze the statistical differences among genotype groups. Compared with the TT subjects at rs7771980 in RUNX2, C-carrier (TC + CC) subjects had a lower vertebral fracture risk after adjusting for age, smoking, alcohol, total calorie intake, total energy expenditure, total calcium intake, total fat intake, weight, body fat. Odds ratio (OR) and 95% interval (CI) for the vertebral fracture risk was 0.55 (95% CI 0.32-0.94). After adjusting for multiple variables, the prevalence of vertebral fracture was highest in GG subjects at rs1501299 in ADIPOQ (p = 0.0473). A high calcium intake (>1000 mg/day) contributed to a high bone mineral density (BMD) in GT + TT subjects at rs1501299 in ADIPOQ (p for interaction = 0.0295). Even if the mechanisms between obesity-related genes and bone health are not fully established, the results of our study revealed the association of certain SNPs from obesity-related genes with BMD or vertebral fracture risk in postmenopausal Korean women.
与肥胖是骨骼保护因素的传统观念相反，最近的流行病学研究表明，体脂可能是骨质疏松症和骨折的危险因素。因此，我们评估了骨质疏松症或椎体骨折的表型与肥胖相关基因，即过氧化物酶体增殖物激活受体γ（PPARG）、 runt相关转录因子2（RUNX2）、瘦素受体（LEPR）和脂联素（ADIPOQ）变体之间的关联。本研究共纳入907名60-79岁的绝经后健康女性。测量了骨密度以及骨骼健康和肥胖的生物标志物。我们对来自四个基因（PPARG、RUNX2、LEPR、ADIPOQ）的四个单核苷酸多态性（SNP）进行了基因分型。使用连续因变量的一般线性模型和分类因变量的逻辑回归模型来分析基因型组之间的统计差异。与RUNX2基因rs7771980位点的TT受试者相比，C携带者（TC + CC）受试者在调整年龄、吸烟、饮酒、总热量摄入、总能量消耗、总钙摄入量、总脂肪摄入量、体重、体脂后椎体骨折风险较低。椎体骨折风险的比值比（OR）和95%可信区间（CI）为0.55（95%CI 0.32-0.94）。调整多个变量后，ADIPOQ基因rs1501299位点的GG受试者椎体骨折患病率最高（p = 0.0473）。高钙摄入量（>1000毫克/天）有助于ADIPOQ基因rs1501299位点的GT + TT受试者获得较高的骨矿物质密度（BMD）（交互作用p = 0.0295）。即使肥胖相关基因与骨骼健康之间的机制尚未完全明确，我们的研究结果揭示了肥胖相关基因的某些SNP与绝经后韩国女性的骨密度或椎体骨折风险之间的关联。
