Ciccarone Center for the Prevention of Cardiovascular Disease Johns Hopkins University School of Medicine Baltimore MD.
Department of Family Medicine University of California San Diego San Diego CA.
J Am Heart Assoc. 2024 Sep 17;13(18):e030548. doi: 10.1161/JAHA.123.030548. Epub 2024 Sep 9.
The metabolic syndrome phenotype of individuals with obesity is characterized by elevated levels of triglyceride-rich lipoproteins and remnant particles, which have been shown to be significantly atherogenic. Understanding the association between adipokines, endogenous hormones produced by adipose tissue, and remnant cholesterol (RC) would give insight into the link between obesity and atherosclerotic cardiovascular disease.
We studied 1791 MESA (Multi-Ethnic Study of Atherosclerosis) participants who took part in an ancillary study on body composition with adipokine levels measured (leptin, adiponectin, and resistin) at either visit 2 or visit 3. RC was calculated as non-high-density lipoprotein cholesterol minus low-density lipoprotein cholesterol, measured at the same visit as the adipokines, as well as subsequent visits 4 through 6. Multivariable-adjusted linear mixed-effects models were used to assess the cross-sectional and longitudinal associations between adipokines and log-transformed levels of RC. Mean±SD age was 64.5±9.6 years; mean±SD body mass index was 29.9±5.0 kg/m; and 52.0% were women. In fully adjusted cross-sectional models that included body mass index, diabetes, low-density lipoprotein cholesterol, and lipid-lowering therapy, for each 1-unit increment in adiponectin, there was 14.6% (95% CI, 12.2-16.9) lower RC. With each 1-unit increment in leptin and resistin, there was 4.8% (95% CI, 2.7-7.0) and 4.0% (95% CI, 0.2-8.1) higher RC, respectively. Lower adiponectin and higher leptin were also associated with longitudinal increases in RC levels over median follow-up of 5 (interquartile range, 4-8) years.
Lower adiponectin and higher leptin levels were independently associated with higher levels of RC at baseline and longitudinal RC increase, even after accounting for body mass index and low-density lipoprotein cholesterol.
肥胖个体的代谢综合征表型的特征是甘油三酯丰富的脂蛋白和残粒水平升高，这些脂蛋白和残粒已被证明具有明显的动脉粥样硬化作用。了解脂肪因子（脂肪组织产生的内源性激素）与残余胆固醇（RC）之间的关系，可以深入了解肥胖与动脉粥样硬化性心血管疾病之间的联系。
我们研究了 1791 名参加 MESA（动脉粥样硬化多民族研究）的参与者，他们参加了一项关于脂肪因子水平测量的辅助身体成分研究（在访视 2 或访视 3 时测量瘦素、脂联素和抵抗素）。RC 计算为非高密度脂蛋白胆固醇减去低密度脂蛋白胆固醇，与脂肪因子同时测量，也与随后的访视 4 至 6 测量。使用多变量调整的线性混合效应模型来评估脂肪因子与 RC 的对数转换水平之间的横断面和纵向关联。平均年龄±标准差为 64.5±9.6 岁；平均体重指数±标准差为 29.9±5.0 kg/m2；52.0%为女性。在包含体重指数、糖尿病、低密度脂蛋白胆固醇和降脂治疗的完全调整的横断面模型中，脂联素每增加 1 个单位，RC 降低 14.6%（95%CI，12.2-16.9）。瘦素和抵抗素每增加 1 个单位，RC 分别增加 4.8%（95%CI，2.7-7.0）和 4.0%（95%CI，0.2-8.1）。脂联素降低和瘦素升高也与 RC 水平的纵向升高相关，中位随访时间为 5 年（四分位距，4-8 年）。
即使在考虑体重指数和低密度脂蛋白胆固醇后，较低的脂联素和较高的瘦素水平与基线时 RC 水平较高以及纵向 RC 增加独立相关。
