Transition of metabolic phenotypes and risk of subclinical atherosclerosis according to BMI: a prospective study

Transition of metabolic phenotypes and risk of subclinical atherosclerosis according to BMI: a prospective study
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根据 BMI 的代谢表型转变和亚临床动脉粥样硬化风险:一项前瞻性研究

DOI:
10.1007/s00125-020-05116-5
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发表时间:
2020-07-01
期刊:
影响因子:
8.2
通讯作者:
Chen, Yuhong
Chen, Yuhong
中科院分区:
医学1区
文献类型:
--
作者:
Lin, Lin;Zhang, Jie;Chen, Yuhong

文献摘要

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与代谢健康肥胖(MHO)相关的心脏代谢风险仍然是争论的主题。目前还不清楚MHO是否是一种影响亚临床动脉粥样硬化风险的短暂性疾病。在本研究中,我们的目的是研究MHO及其随时间推移的转变与亚临床动脉粥样硬化事件的相关性。方法对6220例基线时无心血管疾病(CVD)的中国成年人进行前瞻性研究。肥胖定义为BMI ≥ 25.0 kg/m2。代谢健康被定义为一个人有不到两个国家胆固醇教育计划专家小组的检测,评估和治疗高血胆固醇的成人(NCEP ATP III)标准的代谢综合征的组成部分(不包括腰围)。亚临床动脉粥样硬化通过臂踝脉搏波速度、脉压和蛋白尿单独或联合测量。参与者通过BMI类别和代谢健康状况及其在随访期间的转变进行交叉分类。使用逆概率加权逻辑回归模型估计亚临床动脉粥样硬化的OR和95%CI。结果MHO表型占总人群的16.3%,占基线肥胖人群的32.8%。基线MHO与亚临床动脉粥样硬化事件无显著相关性。在4.4年的随访期间,46.8%的MHO患者出现了代谢不健康状态。与代谢健康的非肥胖参考组相比,一过性MHO患者发生复合亚临床动脉粥样硬化的风险增加(OR 2.52 [95%CI 1.89,3.36])。从代谢不健康状态到健康状态的转变被证明可以降低结局风险。BMI与亚临床动脉粥样硬化的关系部分由血压和血糖介导。结论/解释MHO不是一种稳定的疾病,短暂的MHO增加了亚临床动脉粥样硬化(CVD的早期阶段)的风险。因此,个人可能受益于早期的行为或医疗管理,以避免代谢状态的恶化和预防动脉粥样硬化和CVD。
Aims/hypothesis The cardiometabolic risk associated with metabolically healthy obesity (MHO) remains the subject of debate. It is unclear whether MHO is a transient condition that affects subclinical atherosclerosis risk. In this study, we aimed to investigate the association of MHO and its transition over time with incident subclinical atherosclerosis. Methods A prospective study was conducted with 6220 Chinese adults who were free of cardiovascular disease (CVD) at baseline. Obesity was defined as BMI >= 25.0 kg/m(2). Metabolic health was defined as an individual having fewer than two of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) criteria for components of the metabolic syndrome (excluding waist circumference). Subclinical atherosclerosis was measured by brachial-ankle pulse wave velocity, pulse pressure and albuminuria, separately or combined. Participants were cross-classified by BMI categories and by metabolic health status and its transition during follow-up. Inverse probability weighted logistic regression models were used to estimate ORs and 95% CIs for subclinical atherosclerosis. Results The MHO phenotype accounted for 16.3% of the total population and 32.8% of the population with obesity at baseline. Baseline MHO was not significantly associated with incident subclinical atherosclerosis. During a follow-up period of 4.4 years, 46.8% of individuals with MHO developed a metabolically unhealthy status. Those with transient MHO had an increased risk of composite subclinical atherosclerosis compared with those in the metabolically healthy non-obesity reference group (OR 2.52 [95% CI 1.89, 3.36]). A transition from metabolically unhealthy to healthy status was shown to decrease the outcome risk. The relationship between BMI and subclinical atherosclerosis was partly mediated by BP and plasma glucose. Conclusions/interpretation MHO is not a stable condition and transient MHO conferred an increased risk of subclinical atherosclerosis, the early stage of CVD. Hence, individuals may benefit from early behavioural or medical management in order to avoid a deterioration of metabolic status and prevent atherosclerosis and CVD.