Severity of sleep apnea impairs adipose tissue insulin sensitivity in individuals with obesity and newly diagnosed obstructive sleep apnea

Sara Rodrigues, Luiz Aparecido Bortolotto, Robbie A. Beyl, Prachi Singh
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Abstract

Introduction Obstructive sleep apnea (OSA) is a common sleep disorder associated with increased risk for the development of type 2 diabetes. While studies have examined the effects of sleep on whole-body insulin sensitivity, little is known about the effects of sleep on adipose tissue insulin sensitivity in patients with OSA. We analyzed if the severity of OSA, measured by apnea-hypopnea index (AHI), is associated with adipose tissue insulin sensitivity. Methods We examined the relationship between sleep parameters and adipose tissue insulin sensitivity in non-diabetic participants with obesity and newly diagnosed OSA who underwent overnight polysomnography and a 2 h oral glucose tolerance test during which circulating free fatty acids were measured. In total, 16 non-diabetic participants with obesity and newly diagnosed OSA (sex, 81.3% males; mean age, 50.9 ± 6.7 y; BMI, 36.5 ± 2.9 kg/m 2 ; AHI, 43 ± 20 events/h) were included in the analysis. Results In our study participants, AHI is inversely associated with free-fatty acid suppression during oral glucose challenge ( R = −0.764, p = 0.001). This relationship persisted even after statistical adjustment for age ( R = −0.769, p = 0.001), body mass index ( R = −0.733, p = 0.002), waist-to-hip ratio ( R = −0.741, p = 0.004), or percent body fat mass ( R = −0.0529, p = 0.041). Furthermore, whole-body insulin sensitivity as determined by the Matsuda index was associated with percent REM sleep ( R = 0.552, p = 0.027) but not AHI ( R = −0.119, p = 0.660). Conclusion In non-diabetic patients with OSA, the severity of sleep apnea is associated with adipose tissue insulin sensitivity but not whole-body insulin sensitivity. The impairments in adipose tissue insulin sensitivity may contribute to the development of type 2 diabetes.
睡眠呼吸暂停的严重程度损害肥胖和新诊断的阻塞性睡眠呼吸暂停个体的脂肪组织胰岛素敏感性
阻塞性睡眠呼吸暂停(OSA)是一种常见的睡眠障碍,与2型糖尿病的发病风险增加有关。虽然研究已经检查了睡眠对全身胰岛素敏感性的影响,但睡眠对OSA患者脂肪组织胰岛素敏感性的影响知之甚少。我们分析了通过呼吸暂停低通气指数(AHI)测量的OSA严重程度是否与脂肪组织胰岛素敏感性相关。方法我们研究了睡眠参数与脂肪组织胰岛素敏感性之间的关系,这些非糖尿病肥胖和新诊断的OSA参与者接受了夜间多导睡眠图和2小时口服葡萄糖耐量试验,在此期间测量了循环游离脂肪酸。共有16名患有肥胖症和新诊断的OSA的非糖尿病参与者(性别,81.3%男性;平均年龄50.9±6.7岁;BMI: 36.5±2.9 kg/ m2;AHI(43±20事件/小时)纳入分析。在我们的研究参与者中,在口服葡萄糖刺激期间,AHI与游离脂肪酸抑制呈负相关(R = - 0.764, p = 0.001)。即使在年龄(R = - 0.769, p = 0.001)、体重指数(R = - 0.733, p = 0.002)、腰臀比(R = - 0.741, p = 0.004)、体脂率(R = - 0.0529, p = 0.041)等因素进行统计调整后,这种关系仍然存在。此外,由Matsuda指数测定的全身胰岛素敏感性与REM睡眠百分比相关(R = 0.552, p = 0.027),但与AHI无关(R = - 0.119, p = 0.660)。结论非糖尿病OSA患者睡眠呼吸暂停严重程度与脂肪组织胰岛素敏感性相关,与全身胰岛素敏感性无关。脂肪组织胰岛素敏感性的损害可能导致2型糖尿病的发生。
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