Almazov National Medical Research Centre, St Petersburg 197341, Russia.
Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, St Petersburg 194223, Russia.
Int J Mol Sci. 2020 Jun 30;21(13):4680. doi: 10.3390/ijms21134680.
Lipoprotein (a) (Lp(a)) is considered a genetic factor for cardiovascular disease playing an important role in atherogenesis and thrombosis, but the evidence about its association with sleep duration is controversial. We evaluated the relation between self-reported sleep duration and Lp(a). Among 1600 participants of the population-based sample, we selected 1427 subjects without previously known cardiovascular events, who answered the questions about their sleep duration; had valid lipid profile results (total cholesterol, low- and high-density lipoproteins, Lp(a), apolipoprotein AI (ApoAI), ApoB, and ApoB/ApoAI); and did not take lipid-lowering drugs (mean age 46 ± 12 years). We performed a structured interview, which included questions about lifestyle, medical history, complaints, and sleep duration (How long have you been sleeping per night during the last month?). Sleep duration was classified as follows: <6 h/night-short, 6-9 h/night-normal, and ≥10 h/night-long. Overall, 73 respondents (5.2%) were short-sleepers and 69 (4.8%) long-sleepers. Males were slightly more prevalent among short-sleepers. The groups matched by age, body mass index, blood pressure, diabetes mellitus, and hypertension rate. Short-sleepers had lower rates of high total cholesterol (≥5.0 mmol/L), lower Lp(a) levels and lower rates of increased Lp(a) ≥0.5 g/L, and higher insulin and insulin resistance (assessed by the homeostatic model assessment for insulin resistance (HOMA-IR)). ApoAI, ApoB, their ratio, and other lab tests were similar in the groups. The multinomial logistic regression demonstrated that only the short sleep duration was independently (odds ratio (OR) 0.29, 95% confidence interval (CI) (0.09-0.91), = 0.033) associated with Lp(a) (χ = 41.58, = 0.003). Other influencing factors were smoking and HOMA-IR. Such an association was not found for long-sleepers. In conclusion, a short-sleep duration is associated with Lp(a). The latter might mediate the higher insulin resistance and higher cardiometabolic risks in short-sleepers.
脂蛋白 (a) (Lp(a)) 被认为是心血管疾病的遗传因素，在动脉粥样硬化和血栓形成中发挥重要作用，但关于其与睡眠时间的关系的证据仍存在争议。我们评估了自我报告的睡眠时间与 Lp(a) 之间的关系。在基于人群的样本中，我们从 1600 名参与者中选择了 1427 名没有先前已知心血管事件的受试者，他们回答了关于睡眠时长的问题；具有有效的血脂谱结果（总胆固醇、低和高密度脂蛋白、Lp(a)、载脂蛋白 AI (ApoAI)、载脂蛋白 B (ApoB) 和 ApoB/ApoAI)；并且没有服用降脂药物（平均年龄 46 ± 12 岁）。我们进行了一项结构访谈，其中包括关于生活方式、病史、抱怨和睡眠时长的问题（过去一个月每晚睡多长时间？）。睡眠时间分类如下：每晚睡眠 <6 小时 - 短，每晚睡眠 6-9 小时 - 正常，每晚睡眠 ≥10 小时 - 长。共有 73 名受访者（5.2%）为短睡眠者，69 名（4.8%）为长睡眠者。短睡眠者中男性略多。两组在年龄、体重指数、血压、糖尿病和高血压发生率方面相匹配。短睡眠者的高总胆固醇（≥5.0mmol/L）发生率较低，Lp(a) 水平较低，Lp(a) 增加（≥0.5g/L）的发生率较低，胰岛素和胰岛素抵抗（通过稳态模型评估胰岛素抵抗（HOMA-IR））较高。ApoAI、ApoB、它们的比值和其他实验室检查在两组中相似。多变量逻辑回归表明，只有短睡眠时间与 Lp(a) 独立相关（比值比 (OR) 0.29，95%置信区间 (CI) (0.09-0.91)， = 0.033）（χ = 41.58， = 0.003）。其他影响因素是吸烟和 HOMA-IR。长睡眠者则没有这种关联。总之，短睡眠时间与 Lp(a) 有关。后者可能介导了短睡眠者更高的胰岛素抵抗和更高的心血管代谢风险。
