Lam Jamie C M, Xu Aimin, Tam Sidney, Khong Pek-Ian, Yao Tzy-Jyun, Lam David C L, Lai Agnes Y K, Lam Bing, Lam Karen S L, Mary S M
Department of Medicine, Queen Mary Hospital, Hong Kong, SAR China.
Sleep. 2008 Dec;31(12):1721-7. doi: 10.1093/sleep/31.12.1721.
Hypoadiponectinemia is associated with cardiovascular morbidity and diabetes mellitus. We hypothesize that adiponectin may be downregulated in sleep apnea through various mechanisms, contributing to cardiometabolic risks. This study investigated the relationship between serum adiponectin and sleep disordered breathing and its potential determinants.
Cross-sectional study.
Adult men without prevailing medical comorbidity from the sleep clinic in a teaching hospital.
MEASUREMENTS & RESULTS: One hundred thirty-four men underwent polysomnography, with mean age of 43.9 (9.8) years, and median apnea-hypopnea index (AHI) of 17.1 (5.7, 46.6). Overnight urine samples for catecholamines and blood samples for analyses of insulin, glucose and adiponectin levels from fasting subjects were taken. Insulin resistance was estimated by homeostasis model assessment (HOMA-IR). Magnetic resonance imaging was performed to quantify the amount of abdominal visceral fat. Serum adiponectin level, adjusted for age, body mass index, and visceral fat volume, was significantly lower in subjects with severe obstructive sleep apnea (AHI > or =30) compared with those with an AHI of less than 30: 4.0 (3.1, 5.4) versus 5.4 (3.6, 7.9) microg/mL, P = 0.039. After we adjusted for adiposity, adiponectin levels remained negatively correlated with AHI (P = 0.037), arousal index (P = 0.022), HOMA-IR/fasting insulin (P < 0.001), and urinary norepinephrine and normetanephrine (P < 0.008). In a multiple stepwise regression model, the independent determinants of adiponectin after adjustment for adiposity were HOMA-IR (P < 0.001) and urinary norepinephrine and normetanephrine (P = 0.037).
Adiponectin was suppressed in subjects with severe obstructive sleep apnea, independent of obesity. Adiponectin levels were determined by insulin resistance and sympathetic activation, factors that may be totally or partially attributed to sleep disordered breathing.
低脂联素血症与心血管疾病和糖尿病相关。我们推测睡眠呼吸暂停可能通过多种机制导致脂联素下调，进而增加心脏代谢风险。本研究调查了血清脂联素与睡眠呼吸紊乱之间的关系及其潜在决定因素。
横断面研究。
来自教学医院睡眠门诊的无主要内科合并症的成年男性。
134名男性接受了多导睡眠图检查，平均年龄43.9（9.8）岁，呼吸暂停低通气指数（AHI）中位数为17.1（5.7，46.6）。采集过夜尿样检测儿茶酚胺，采集空腹受试者血样分析胰岛素、血糖和脂联素水平。通过稳态模型评估（HOMA-IR）估算胰岛素抵抗。进行磁共振成像以量化腹部内脏脂肪量。校正年龄、体重指数和内脏脂肪体积后，重度阻塞性睡眠呼吸暂停（AHI≥30）患者的血清脂联素水平显著低于AHI小于30的患者：4.0（3.1，5.4）对5.4（3.6，7.9）μg/mL，P = 0.039。校正肥胖因素后，脂联素水平仍与AHI（P = 0.037）、觉醒指数（P = 0.022）、HOMA-IR/空腹胰岛素（P < 0.001）以及尿去甲肾上腺素和去甲变肾上腺素（P < 0.008）呈负相关。在多元逐步回归模型中，校正肥胖因素后，脂联素的独立决定因素为HOMA-IR（P < 0.001）以及尿去甲肾上腺素和去甲变肾上腺素（P = 0.037）。
重度阻塞性睡眠呼吸暂停患者的脂联素受到抑制，与肥胖无关。脂联素水平由胰岛素抵抗和交感神经激活决定，这些因素可能全部或部分归因于睡眠呼吸紊乱。
