Polotsky Vsevolod Y, Patil Susheel P, Savransky Vladimir, Laffan Alison, Fonti Shannon, Frame Leigh A, Steele Kimberly E, Schweizter Michael A, Clark Jeanne M, Torbenson Michael S, Schwartz Alan R
Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA.
Am J Respir Crit Care Med. 2009 Feb 1;179(3):228-34. doi: 10.1164/rccm.200804-608OC. Epub 2008 Oct 31.
Obstructive sleep apnea is associated with insulin resistance and liver injury. It is unknown whether apnea contributes to insulin resistance and steatohepatitis in severe obesity.
To examine whether sleep apnea and nocturnal hypoxemia predict the severity of insulin resistance, systemic inflammation, and steatohepatitis in severely obese individuals presenting for bariatric surgery.
We performed sleep studies and measured fasting blood glucose, serum insulin, C-reactive protein, and liver enzymes in 90 consecutive severely obese individuals, 75 women and 15 men, without concomitant diabetes mellitus or preexistent diagnosis of sleep apnea or liver disease. Liver biopsies (n = 20) were obtained during bariatric surgery.
Obstructive sleep apnea with a respiratory disturbance index greater than 5 events/hour was diagnosed in 81.1% of patients. The median respiratory disturbance index was 15 +/- 29 events/hour and the median oxygen desaturation during apneic events was 4.6 +/- 1.8%. All patients exhibited high serum levels of C-reactive protein, regardless of the severity of apnea, whereas liver enzymes were normal. Oxygen desaturation greater than 4.6% was associated with a 1.5-fold increase in insulin resistance, according to the homeostasis model assessment index. Histopathology data suggested that significant nocturnal desaturation might predispose to hepatic inflammation, hepatocyte ballooning, and liver fibrosis. Fasting blood glucose levels and steatosis scores were not affected by nocturnal hypoxia. There was no relationship between the respiratory disturbance index and insulin resistance or liver histopathology.
Hypoxic stress of sleep apnea may be implicated in the development of insulin resistance and steatohepatitis in severe obesity.
阻塞性睡眠呼吸暂停与胰岛素抵抗和肝损伤有关。目前尚不清楚呼吸暂停是否会导致严重肥胖患者出现胰岛素抵抗和脂肪性肝炎。
研究睡眠呼吸暂停和夜间低氧血症是否可预测接受减肥手术的严重肥胖个体的胰岛素抵抗、全身炎症和脂肪性肝炎的严重程度。
我们对90例连续的严重肥胖个体（75名女性和15名男性）进行了睡眠研究，并测量了空腹血糖、血清胰岛素、C反应蛋白和肝酶，这些个体均无糖尿病合并症，也未预先诊断为睡眠呼吸暂停或肝病。在减肥手术期间获取了肝活检样本（n = 20）。
81.1%的患者被诊断为呼吸紊乱指数大于5次/小时的阻塞性睡眠呼吸暂停。呼吸紊乱指数的中位数为15±29次/小时，呼吸暂停事件期间的氧饱和度下降中位数为4.6±1.8%。所有患者的C反应蛋白血清水平均较高，无论呼吸暂停的严重程度如何，而肝酶均正常。根据稳态模型评估指数，氧饱和度下降大于4.6%与胰岛素抵抗增加1.5倍相关。组织病理学数据表明，显著的夜间氧饱和度下降可能易导致肝脏炎症、肝细胞气球样变和肝纤维化。空腹血糖水平和脂肪变性评分不受夜间低氧的影响。呼吸紊乱指数与胰岛素抵抗或肝脏组织病理学之间无相关性。
睡眠呼吸暂停的低氧应激可能与严重肥胖患者胰岛素抵抗和脂肪性肝炎的发生有关。
