Labouesse Marie A, Gertz Erik R, Piccolo Brian D, Souza Elaine C, Schuster Gertrud U, Witbracht Megan G, Woodhouse Leslie R, Adams Sean H, Keim Nancy L, Van Loan Marta D
AgroParisTech, Paris Institute of Science and Technology, for Life, Food and Environmental Sciences, Paris, France.
Obesity & Metabolism Research Unit, USDA, ARS, Western Human Nutrition Research Center, 430 West Health Sciences Drive, Davis, CA, USA.
Bone. 2014 Jul;64:138-46. doi: 10.1016/j.bone.2014.03.047. Epub 2014 Apr 4.
Weight loss reduces co-morbidities of obesity, but decreases bone mass.
Our aims were to (1) determine if adequate dairy intake attenuates weight loss-induced bone loss; (2) evaluate the associations of endocrine, inflammatory and bone markers, anthropometric and other parameters to bone mineral density and content (BMD, BMC) pre- and post-weight loss; and (3) model the contribution of these variables to post weight-loss BMD and BMC.
Overweight/obese women (BMI: 28-37 kg/m2) were enrolled in an energy reduced (-500 kcal/d; -2092 kJ/d) diet with adequate dairy (AD: 3-4 servings/d; n=25, 32.2±8.8 years) or low dairy (LD: ≤1 serving/d; n=26, 31.7±8.4 years). BMD, BMC and body composition were measured by DXA. Bone markers (CTX, PYD, BAP, OC), endocrine (PTH, vitamin D, leptin, adiponectin, ghrelin, amylin, insulin, GLP-1, PAI-1, HOMA) and inflammatory markers (CRP, IL1-β, IL-6, IL-8, TNF-α, cortisol) were measured in serum or plasma. PA was assessed by accelerometry.
Following weight loss, AD intake resulted in significantly greater (p=0.004) lumbar spine BMD and serum osteocalcin (p=0.004) concentration compared to LD. Pre- and post-body fat was negatively associated with hip and lumbar spine BMC (r=-0.28, p=0.04 to -0.45, p=0.001). Of note were the significant negative associations among bone markers and IL-1β, TNFα and CRP ranging from r = -0.29 (p=0.04) to r = -0.34 (p=0.01); magnitude of associations did not change with weight loss. Adiponectin was negatively related to change in osteocalcin. Factor analysis resulted in 8 pre- and post-weight loss factors. Pre-weight loss factors accounted for 13.7% of the total variance in pre-weight loss hip BMD; post-weight loss factors explained 19.6% of the total variance in post-weight loss hip BMD. None of the factors contributed to the variance in lumbar spine BMD.
AD during weight loss resulted in higher lumbar spine BMD and osteocalcin compared to LD. Significant negative associations were observed between bone and inflammatory markers suggesting that inflammation suppresses bone metabolism. Using factor analysis, 19.6% of total variance in post-weight loss hip BMD could be explained by endocrine, immune, and anthropometric variables, but not lumbar spine BMD.
体重减轻可降低肥胖的合并症，但会减少骨量。
我们的目标是：（1）确定充足的乳制品摄入量是否能减轻体重减轻引起的骨质流失；（2）评估内分泌、炎症和骨标志物、人体测量学及其他参数与体重减轻前后骨矿物质密度和含量（BMD、BMC）之间的关联；（3）模拟这些变量对体重减轻后BMD和BMC的影响。
超重/肥胖女性（BMI：28 - 37 kg/m²）参与了能量减少（-500 kcal/d；-2092 kJ/d）的饮食计划，其中一组摄入充足的乳制品（AD：3 - 4份/天；n = 25，32.2±8.8岁），另一组摄入少量乳制品（LD：≤1份/天；n = 26，31.7±8.4岁）。通过双能X线吸收法（DXA）测量BMD、BMC和身体成分。在血清或血浆中测量骨标志物（CTX、PYD、BAP、OC）、内分泌指标（PTH、维生素D、瘦素、脂联素、胃饥饿素、胰淀素、胰岛素、GLP - 1、PAI - 1、HOMA）和炎症标志物（CRP、IL1 - β、IL - 6、IL - 8、TNF - α、皮质醇）。通过加速度计评估身体活动（PA）。
体重减轻后，与LD组相比，AD组的腰椎BMD和血清骨钙素浓度显著更高（p = 0.004）。体重前后的体脂与髋部和腰椎的BMC呈负相关（r = -0.28，p = 0.04至 -0.45，p = 0.001）。值得注意的是，骨标志物与IL - 1β、TNFα和CRP之间存在显著的负相关，范围从r = -0.29（p = 0.04）到r = -0.34（p = 0.01）；随着体重减轻，关联程度没有变化。脂联素与骨钙素的变化呈负相关。因子分析产生了8个体重减轻前后的因子。体重减轻前的因子占体重减轻前髋部BMD总方差的13.7%；体重减轻后的因子解释了体重减轻后髋部BMD总方差的19.6%。没有一个因子对腰椎BMD的方差有贡献。
与LD组相比，体重减轻期间摄入AD导致更高的腰椎BMD和骨钙素。在骨标志物与炎症标志物之间观察到显著的负相关，表明炎症抑制骨代谢。使用因子分析，内分泌、免疫和人体测量学变量可解释体重减轻后髋部BMD总方差的19.6%，但不能解释腰椎BMD。
