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超重和肥胖青少年的睡眠障碍性呼吸、全身脂肪因子分泌和代谢失调。

Sleep-disordered breathing, systemic adipokine secretion, and metabolic dysregulation in overweight and obese children and adolescents.

机构信息

Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.

Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium; Department of Pediatrics, Antwerp University Hospital, Edegem, Belgium.

出版信息

Sleep Med. 2017 Feb;30:52-56. doi: 10.1016/j.sleep.2015.11.014. Epub 2015 Dec 8.

Abstract

OBJECTIVE

Obstructive sleep apnea (OSA) is common among overweight and obese children, and it is an independent risk factor for developing metabolic syndrome. However, the mechanisms linking OSA and metabolic syndrome are still unclear, but a role for adipose tissue dysfunction caused by intermittent hypoxia has been suggested. Therefore, the goal of this study was to investigate the relationship between OSA and systemic adipokine concentrations in overweight and obese children.

METHODS

We included 164 overweight and obese children in a tertiary center and distributed them in groups based on their obstructive apnea-hypopnea index (111 controls, 28 mild OSA, 25 moderate-to-severe OSA). All subjects underwent polysomnography and a blood sample was taken to determine leptin, adiponectin, tumor necrosis factor alpha, and interleukin-6 levels.

RESULTS

No significant differences were found in adipokine levels between subjects with or without OSA. Leptin correlated with oxygen desaturation index (r = -0.17, p = 0.03), adiponectin correlated with mean oxygen saturation (r = 0.24, p = 0.002) and with the percentage of sleep time with an oxygen saturation >95% (r = 0.25, p = 0.001). However, these associations did not persist after correction for adiposity. No correlations between interleukin-6 and tumor necrosis factor alpha, and OSA severity were found.

CONCLUSION

These results suggest that serum adipokine levels are mostly dependent on central obesity, while they are not influenced by OSA in an obese pediatric population.

摘要

目的

阻塞性睡眠呼吸暂停(OSA)在超重和肥胖儿童中较为常见,是代谢综合征发生的独立危险因素。然而,将 OSA 与代谢综合征联系起来的机制尚不清楚,但间歇性低氧引起的脂肪组织功能障碍的作用已被提出。因此,本研究的目的是探讨超重和肥胖儿童中 OSA 与全身脂肪因子浓度之间的关系。

方法

我们纳入了一家三级中心的 164 名超重和肥胖儿童,并根据其阻塞性呼吸暂停-低通气指数将其分组(111 名对照组,28 名轻度 OSA,25 名中重度 OSA)。所有受试者均行多导睡眠图检查,并采集血样以测定瘦素、脂联素、肿瘤坏死因子-α和白细胞介素-6 水平。

结果

OSA 患儿和无 OSA 患儿的脂肪因子水平无显著差异。瘦素与氧减指数呈负相关(r=-0.17,p=0.03),脂联素与平均氧饱和度呈正相关(r=0.24,p=0.002),与氧饱和度>95%的睡眠时间百分比呈正相关(r=0.25,p=0.001)。然而,在对肥胖进行校正后,这些相关性不再存在。白细胞介素-6 和肿瘤坏死因子-α与 OSA 严重程度之间无相关性。

结论

这些结果表明,血清脂肪因子水平主要取决于中心性肥胖,而在肥胖儿童人群中,OSA 并不影响脂肪因子水平。

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