Rutter Martin K, Sullivan Lisa M, Fox Caroline S, Wilson Peter W F, Nathan David M, Vasan Ramachandran S, D'Agostino Ralph B, Meigs James B
1 The Endocrinology and Diabetes Research Group, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester , and Manchester Diabetes Centre, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom .
Metab Syndr Relat Disord. 2014 Sep;12(7):372-80. doi: 10.1089/met.2013.0148. Epub 2014 Jul 9.
Multiple abnormal metabolic traits are found together or "cluster" within individuals more often than is predicted by chance. The individual and combined role of adiposity and insulin resistance (IR) on metabolic trait clustering is uncertain. We tested the hypothesis that change in trait clustering is a function of both baseline level and change in these measures.
In 2616 nondiabetic Framingham Offspring Study participants, body mass index (BMI) and fasting insulin were related to a within-person 7-year change in a trait score of 0-4 Adult Treatment Panel III metabolic syndrome traits (hypertension, high triglycerides, low high-density lipoprotein cholesterol, hyperglycemia).
At baseline assessment, mean trait score was 1.4 traits, and 7-year mean (SEM) change in trait score was +0.25 (0.02) traits, P<0.0001. In models with BMI predictors only, for every quintile difference in baseline BMI, the 7-year trait score increase was 0.14 traits, and for every quintile increase in BMI during 7-year follow-up, the trait score increased by 0.3 traits. Baseline level and change in fasting insulin were similarly related to trait score change. In models adjusted for age-sex-baseline cluster score, 7-year change in trait score was significantly related to both a 1-quintile difference in baseline BMI (0.07 traits) and fasting insulin (0.18 traits), and to both a 1-quintile 7-year increase in BMI (0.21 traits) and fasting insulin (0.18 traits).
Change in metabolic trait clustering was significantly associated with baseline levels and changes in both BMI and fasting insulin, highlighting the importance of both obesity and IR in the clustering of metabolic traits.
多种异常代谢特征在个体中同时出现或“聚集”的频率高于随机预期。肥胖和胰岛素抵抗（IR）对代谢特征聚集的个体及联合作用尚不确定。我们检验了这样一个假设，即特征聚集的变化是这些指标基线水平和变化的函数。
在2616名非糖尿病的弗雷明汉后代研究参与者中，体重指数（BMI）和空腹胰岛素与个体7年内0至4个成人治疗小组III代谢综合征特征（高血压、高甘油三酯、低高密度脂蛋白胆固醇、高血糖）的特征评分变化相关。
在基线评估时，平均特征评分为1.4个特征，7年特征评分的平均（标准误）变化为+0.25（0.02）个特征，P<0.0001。在仅以BMI为预测指标的模型中，基线BMI每相差一个五分位数，7年特征评分增加0.14个特征；在7年随访期间BMI每增加一个五分位数，特征评分增加0.3个特征。空腹胰岛素的基线水平和变化与特征评分变化的关系类似。在根据年龄、性别、基线聚类评分进行校正的模型中，7年特征评分变化与基线BMI相差一个五分位数（0.07个特征）和空腹胰岛素（0.18个特征）均显著相关，与7年中BMI增加一个五分位数（0.21个特征）和空腹胰岛素增加一个五分位数（0.18个特征）也均显著相关。
代谢特征聚集的变化与BMI和空腹胰岛素的基线水平及变化均显著相关，突出了肥胖和IR在代谢特征聚集中的重要性。
