Rodrigues Sara, Bortolotto Luiz Aparecido, Beyl Robbie A, Singh Prachi
Pennington Biomedical Research Center, Baton Rouge, LA, United States.
Unidade de Hipertensao, Instituto do Coracao (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, São Paulo, Brazil.
Front Sleep. 2023;2. doi: 10.3389/frsle.2023.1295301. Epub 2023 Nov 9.
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.
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; AHI, 43 ± 20 events/h) were included in the analysis.
In our study participants, AHI is inversely associated with free-fatty acid suppression during oral glucose challenge ( = -0.764, = 0.001). This relationship persisted even after statistical adjustment for age ( = -0.769, = 0.001), body mass index ( = -0.733, = 0.002), waist-to-hip ratio ( = -0.741, = 0.004), or percent body fat mass ( = -0.0529, = 0.041). Furthermore, whole-body insulin sensitivity as determined by the Matsuda index was associated with percent REM sleep ( = 0.552, = 0.027) but not AHI ( = -0.119, = 0.660).
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.
阻塞性睡眠呼吸暂停(OSA)是一种常见的睡眠障碍,与2型糖尿病发生风险增加相关。虽然已有研究探讨了睡眠对全身胰岛素敏感性的影响,但对于OSA患者睡眠对脂肪组织胰岛素敏感性的影响知之甚少。我们分析了以呼吸暂停低通气指数(AHI)衡量的OSA严重程度是否与脂肪组织胰岛素敏感性相关。
我们研究了肥胖且新诊断为OSA的非糖尿病参与者的睡眠参数与脂肪组织胰岛素敏感性之间的关系,这些参与者接受了夜间多导睡眠监测和2小时口服葡萄糖耐量试验,试验期间测量了循环游离脂肪酸。总共16名肥胖且新诊断为OSA的非糖尿病参与者(性别,81.3%为男性;平均年龄,50.9±6.7岁;BMI,36.5±2.9kg/m²;AHI,43±20次/小时)纳入分析。
在我们的研究参与者中,AHI与口服葡萄糖激发试验期间游离脂肪酸抑制呈负相关(r = -0.764,P = 0.001)。即使在对年龄(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)或体脂百分比(r = -0.529,P = 0.041)进行统计调整后,这种关系仍然存在。此外,由松田指数确定的全身胰岛素敏感性与快速眼动睡眠百分比相关(r = 0.552,P = 0.027),但与AHI无关(r = -0.119,P = 0.660)。
在非糖尿病OSA患者中,睡眠呼吸暂停的严重程度与脂肪组织胰岛素敏感性相关,但与全身胰岛素敏感性无关。脂肪组织胰岛素敏感性受损可能导致2型糖尿病的发生。