Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil.
Department of Physiology and Pharmacology, Federal University of Pelotas, Pelotas, Brazil.
Int J Epidemiol. 2017 Dec 1;46(6):2044-2055. doi: 10.1093/ije/dyx022.
The substantial reduction in adiponectin concentration among obese individuals seems to depend on fat distribution and is a marker of metabolic and adipose tissue dysfunction. We aimed to: (i) address whether abdominal fat from different compartments (visceral, deep subcutaneous abdominal and superficial subcutaneous abdominal) and gluteofemoral fat are independently associated with blood adiponectin concentration; and (ii) investigate whether abdominal (proxied by waist circumference) and gluteofemoral fat (proxied by hip circumference) accumulation causally determine blood adiponectin concentration.
To investigate the independent association of abdominal and gluteofemoral fat with adiponectin concentration, we used multivariable regression and data from 30-year-old adults from the 1982 Pelotas Birth Cohort (n = 2,743). To assess the causal role of abdominal and gluteofemoral fat accumulation on adiponectin concentration, we used Mendelian randomization and data from two consortia of genome-wide association studies-the GIANT (n > 210 000) and ADIPOGen consortia (n = 29 347).
In the multivariable regression analysis, all abdominal fat depots were negatively associated with adiponectin concentration, specially visceral abdominal fat [men: β = -0.24 standard unit of log adiponectin per standard unit increase in abdominal fat; 95% confidence interval (CI) = -0.31, -0.18; P = 810-13; women: β = -0.31; 95% CI = -0.36, -0.25; P = 710-27), whereas gluteofemoral fat was positively associated with adiponectin concentration (men: β = 0.13 standard unit of log adiponectin per standard unit increase in gluteofemoral fat; 95% CI = 0.03, 0.22; P = 0.008; women: β = 0.24; 95% CI = 0.17, 0.31; P = 710-11). In the Mendelian randomization analysis, genetically-predicted waist circumference was inversely related to blood adiponectin concentration (β = -0.27 standard unit of log adiponectin per standard unit increase in waist circumference; 95% CI = -0.36, -0.19; P = 210-11), whereas genetically-predicted hip circumference was positively associated with blood adiponectin concentration (β = 0.17 standard unit of log adiponectin per standard unit increase in hip circumference; 95% CI = 0.11, 0.24; P = 1*10-7).
These results support the hypotheses that there is a complex interplay between body fat distribution and circulating adiponectin concentration, and that whereas obesity-induced hypoadiponectinaemia seems to be primarily attributed to abdominal fat accumulation, gluteofemoral fat accumulation is likely to exert a protective effect.
肥胖个体中脂联素浓度的显著降低似乎取决于脂肪分布，是代谢和脂肪组织功能障碍的标志物。我们旨在：（i）探讨不同部位（内脏、深腹部皮下和浅腹部皮下）的腹部脂肪和臀股脂肪是否与血脂联素浓度独立相关；（ii）研究腹部（以腰围为代表）和臀股脂肪（以臀围为代表）的堆积是否会导致血脂联素浓度发生因果变化。
为了研究腹部和臀股脂肪与脂联素浓度的独立相关性，我们使用多变量回归和来自 1982 年佩洛塔斯出生队列的 30 岁成年人的数据（n=2743）。为了评估腹部和臀股脂肪堆积对脂联素浓度的因果作用，我们使用孟德尔随机化和来自两个全基因组关联研究联盟的数据——GIANT（n＞210000）和 ADIPOGen 联盟（n=29347）。
在多变量回归分析中，所有腹部脂肪均与脂联素浓度呈负相关，特别是内脏腹部脂肪[男性：β=-0.24 个标准单位的对数脂联素/腹部脂肪增加一个标准单位；95%置信区间（CI）=-0.31，-0.18；P=810-13；女性：β=-0.31；95%CI=-0.36，-0.25；P=710-27），而臀股脂肪与脂联素浓度呈正相关（男性：β=0.13 个标准单位的对数脂联素/臀股脂肪增加一个标准单位；95%CI=0.03，0.22；P=0.008；女性：β=0.24；95%CI=0.17，0.31；P=710-11）。在孟德尔随机化分析中，遗传预测的腰围与血脂联素浓度呈负相关（β=-0.27 个标准单位的对数脂联素/腰围增加一个标准单位；95%CI=-0.36，-0.19；P=210-11），而遗传预测的臀围与血脂联素浓度呈正相关（β=0.17 个标准单位的对数脂联素/臀围增加一个标准单位；95%CI=0.11，0.24；P=1*10-7）。
这些结果支持这样的假设，即体脂分布和循环脂联素浓度之间存在复杂的相互作用，而肥胖引起的脂联素减少似乎主要归因于腹部脂肪堆积，而臀股脂肪堆积可能产生保护作用。
