Walsh Jennifer S, Evans Amy L, Bowles Simon, Naylor Kim E, Jones Kerry S, Schoenmakers Inez, Jacques Richard M, Eastell Richard
Academic Unit of Bone Metabolism and
Academic Unit of Bone Metabolism and.
Am J Clin Nutr. 2016 Jun;103(6):1465-71. doi: 10.3945/ajcn.115.120139. Epub 2016 May 11.
The mechanism and clinical significance of low circulating 25-hydroxyvitamin D [25(OH)D] in obese people are unknown. Low total 25(OH)D may be due to low vitamin D-binding proteins (DBPs) or faster metabolic clearance. However, obese people have a higher bone mineral density (BMD), which suggests that low 25(OH)D may not be associated with adverse consequences for bone.
We sought to determine whether 1) vitamin D metabolism and 2) its association with bone health differ by body weight.
We conducted a cross-sectional observational study of 223 normal-weight, overweight, and obese men and women aged 25-75 y in South Yorkshire, United Kingdom, in the fall and spring. A subgroup of 106 subjects was also assessed in the winter. We used novel techniques, including an immunoassay for free 25(OH)D, a stable isotope for the 25(OH)D3 half-life, and high-resolution quantitative tomography, to make a detailed assessment of vitamin D physiology and bone health.
Serum total 25(OH)D was lower in obese and overweight subjects than in normal-weight subjects in the fall and spring (geometric means: 45.0 and 40.8 compared with 58.6 nmol/L, respectively; P < 0.001) but not in the winter. Serum 25(OH)D was inversely correlated with body mass index (BMI) in the fall and spring and in the winter. Free 25(OH)D and 1,25-dihydroxyvitamin D [1,25(OH)2D] were lower in obese subjects. DBP, the DBP genotype, and the 25(OH)D3 half-life did not differ between BMI groups. Bone turnover was lower, and bone density was higher, in obese people.
Total and free 25(OH)D and 1,25(OH)2D are lower at higher BMI, which cannot be explained by lower DBP or the shorter half-life of 25(OH)D3 We speculate that low 25(OH)D in obesity is due to a greater pool of distribution. Lower 25(OH)D may not reflect at-risk skeletal health in obese people, and BMI should be considered when interpreting serum 25(OH)D as a marker of vitamin D status.
肥胖人群循环中25-羟基维生素D[25(OH)D]水平较低的机制及临床意义尚不清楚。总25(OH)D水平低可能是由于维生素D结合蛋白（DBP）水平低或代谢清除更快。然而，肥胖人群的骨矿物质密度（BMD）较高，这表明低25(OH)D可能与骨骼的不良后果无关。
我们试图确定1）维生素D代谢以及2）其与骨骼健康的关联是否因体重不同而存在差异。
我们在英国南约克郡对223名年龄在25 - 75岁的正常体重、超重和肥胖男性及女性进行了一项横断面观察研究，研究时间为秋季和春季。还在冬季对106名受试者的一个亚组进行了评估。我们使用了新技术，包括游离25(OH)D免疫测定、25(OH)D3半衰期的稳定同位素以及高分辨率定量断层扫描，以详细评估维生素D生理学和骨骼健康。
在秋季和春季，肥胖和超重受试者的血清总25(OH)D低于正常体重受试者（几何均值：分别为45.0和40.8，而正常体重受试者为58.6 nmol/L；P < 0.001），但在冬季并非如此。血清25(OH)D在秋季、春季和冬季均与体重指数（BMI）呈负相关。肥胖受试者的游离25(OH)D和1,25-二羟基维生素D[1,25(OH)2D]较低。BMI组之间的DBP、DBP基因型和25(OH)D3半衰期没有差异。肥胖人群的骨转换较低，骨密度较高。
BMI较高时，总25(OH)D、游离25(OH)D和1,25(OH)2D较低，这无法用较低的DBP或25(OH)D3较短的半衰期来解释。我们推测肥胖中低25(OH)D是由于分布池更大。较低的25(OH)D可能并不反映肥胖人群骨骼健康存在风险，在将血清25(OH)D解释为维生素D状态标志物时应考虑BMI。
Zotero 插件