Zachariah Justin P, Quiroz Rene, Enserro Danielle, Andersson Charlotte, Keaney John F, Sullivan Lisa M, Vasan Ramachandran S
Section of Pediatric Cardiology, Department of Pediatrics, Texas Children's Hospital Baylor College of Medicine, Houston, TX
Cardiology Section, Boston University, Boston, MA.
J Am Heart Assoc. 2017 Jul 16;6(7):e004973. doi: 10.1161/JAHA.116.004973.
Adipokines are implicated in the development of obesity-related traits. We hypothesized that nonobese participants without diabetes mellitus (DM) whose parents were obese or had DM would have altered circulating adipokines compared with those without parental history of these conditions.
Participants in the community-based Framingham Third Generation cohort who were not obese (body mass index <30) and not diabetic with both parents in the Framingham Offspring cohort were included in this analysis (n=2034, mean age 40 years, 54% women). Circulating concentrations of fetuin A, RBP4 (retinol binding protein 4), FABP4 (fatty acid binding protein 4), leptin, LEP-R (leptin receptor), and adiponectin were assayed. Parental DM was defined as occurring before age 60 years, and obesity was defined as body mass index ≥30 before age 60 years. General estimating equations were used to compare concentrations of adipokines among participants with 0, 1, or 2 parents affected by obesity or DM (separate analyses for each), adjusting for known correlates of adipokines. Overall, 44% had at least 1 parent who was obese and 15% had parents with DM. Parental obesity was associated with higher serum levels of FABP4 and LEP-R in their offspring (=0.02 for both). Parental DM was associated with lower adiponectin but higher RBP4 concentrations in offspring (≤0.02 for both).
In our community-based sample, a parental history of DM or obesity was associated with an altered adipokine profile in nonobese nondiabetic offspring. Additional studies are warranted to evaluate whether such preclinical biomarker alterations presage future risk of disease.
脂肪因子与肥胖相关特征的发展有关。我们假设,与没有这些疾病家族史的非肥胖参与者相比,父母肥胖或患有糖尿病(DM)的非肥胖且无糖尿病的参与者循环脂肪因子会发生改变。
本分析纳入了社区动脉粥样硬化风险研究(Framingham)第三代队列中未肥胖(体重指数<30)且无糖尿病且父母均在Framingham后代队列中的参与者(n = 2034,平均年龄40岁,54%为女性)。检测了胎球蛋白A、视黄醇结合蛋白4(RBP4)、脂肪酸结合蛋白4(FABP4)、瘦素、瘦素受体(LEP-R)和脂联素的循环浓度。父母患糖尿病定义为在60岁之前发病,肥胖定义为60岁之前体重指数≥30。使用广义估计方程比较受肥胖或糖尿病影响的父母数量为0、1或2的参与者之间的脂肪因子浓度(对每种情况分别进行分析),并对已知的脂肪因子相关因素进行调整。总体而言,44%的参与者至少有1位父母肥胖,15%的参与者父母患有糖尿病。父母肥胖与后代血清FABP4和LEP-R水平升高相关(两者均P = 0.02)。父母患糖尿病与后代脂联素水平降低但RBP4浓度升高相关(两者均P≤0.02)。
在我们基于社区的样本中,父母有糖尿病或肥胖病史与非肥胖非糖尿病后代的脂肪因子谱改变有关。有必要进行更多研究以评估这种临床前生物标志物改变是否预示未来疾病风险。