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持续气道正压通气治疗可改善阻塞性睡眠呼吸暂停肥胖男性的低脂联素血症,而不改变胰岛素抵抗。

Continuous positive airway pressure therapy improves hypoadiponectinemia in severe obese men with obstructive sleep apnea without changes in insulin resistance.

机构信息

Department of Medicine, Division of Endocrinology, Universidade Federal de São Paulo, São Paulo, Brazil.

出版信息

Metab Syndr Relat Disord. 2009 Dec;7(6):537-42. doi: 10.1089/met.2009.0019.

Abstract

BACKGROUND

Obstructive sleep apnea (OSA) is associated with several conditions that could facilitate the onset of cardiovascular and metabolic dysfunctions. Continuous positive airway pressure (CPAP) therapy has been shown to improve cardiovascular morbidity and mortality related to OSA, but the mechanisms underlying this association are not fully understood.

OBJECTIVE

The aim of the present study was to evaluate whether sleep apnea contributes to insulin resistance and inflammatory marker alterations and to evaluate the benefits of nasal CPAP therapy in severe obese patients with OSA.

METHODS

Plasma inflammatory cytokines and the homeostasis model assessment of insulin resistance index (HOMA-IR, Insulin Sensitivity Index [ISI]) were measured in severe obese male with OSA (n = 16) and compared with body mass index (BMI)-matched male controls without OSA (n = 13). Seven patients with severe sleep apnea (apnea-hypopnea index >30 events/h) were reevaluated after 3 months of nasal CPAP therapy.

RESULTS

OSA patients had a significantly lower adiponectin levels than obese controls (8.7 +/- 1.18 ng/mL vs. 15.0 +/- 2.55 ng/mL, P = 0.025). HOMA-IR, ISI, tumor necrosis factor-alpha (TNF-alpha, C-reactive protein (CRP), and interleukin-6 (IL-6) levels were not different between groups. Although insulin resistance index and BMI values did not change after 3 months of nCPAP therapy, adiponectin levels increased (P = 0.036) and the levels of TNF-alpha tended to decrease (P = 0.065). Changes in adiponectin levels during nCPAP therapy were positively correlated with an improvement in minimum oxygen saturation (r = 0.773; P = 0.041) and negatively correlated with changes in TNF-alpha levels (r = -0.885; P = 0.008).

CONCLUSIONS

nCPAP therapy reverses hypoadiponectinemia levels present in obese men with OSA, probably through reductions in hypoxia and inflammation activity.

摘要

背景

阻塞性睡眠呼吸暂停(OSA)与多种可能导致心血管和代谢功能障碍的病症相关。持续气道正压通气(CPAP)治疗已被证明可改善与 OSA 相关的心血管发病率和死亡率,但这种关联的机制尚不完全清楚。

目的

本研究旨在评估睡眠呼吸暂停是否导致胰岛素抵抗和炎症标志物改变,并评估 CPAP 治疗对患有 OSA 的严重肥胖患者的益处。

方法

测量了 16 名患有 OSA 的严重肥胖男性和 13 名 BMI 匹配的无 OSA 男性对照者的血浆炎症细胞因子和稳态模型评估的胰岛素抵抗指数(HOMA-IR、胰岛素敏感指数[ISI])。7 名严重睡眠呼吸暂停(呼吸暂停-低通气指数>30 次/小时)患者在接受 3 个月 CPAP 治疗后进行了重新评估。

结果

OSA 患者的脂联素水平明显低于肥胖对照组(8.7 +/- 1.18 ng/mL 与 15.0 +/- 2.55 ng/mL,P = 0.025)。两组之间的 HOMA-IR、ISI、肿瘤坏死因子-α(TNF-α)、C 反应蛋白(CRP)和白细胞介素-6(IL-6)水平无差异。尽管 nCPAP 治疗 3 个月后胰岛素抵抗指数和 BMI 值没有变化,但脂联素水平增加(P = 0.036),TNF-α 水平趋于下降(P = 0.065)。nCPAP 治疗期间脂联素水平的变化与最低氧饱和度的改善呈正相关(r = 0.773;P = 0.041),与 TNF-α 水平的变化呈负相关(r = -0.885;P = 0.008)。

结论

nCPAP 治疗可逆转肥胖伴 OSA 男性患者的低脂联素血症水平,可能通过减少缺氧和炎症活动来实现。

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