Newhouse Lauren P, Joyner Michael J, Curry Timothy B, Laurenti Marcello C, Man Chiara Dalla, Cobelli Claudio, Vella Adrian, Limberg Jacqueline K
Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota.
Department of Information Engineering, University of Padua, Padua, Italy.
Physiol Rep. 2017 Jan;5(1). doi: 10.14814/phy2.13106. Epub 2017 Jan 13.
An independent association exists between sleep apnea and diabetes. Animal models suggest exposure to intermittent hypoxia, a consequence of sleep apnea, results in altered glucose metabolism and fasting hyperglycemia. However, it is unknown if acute exposure to intermittent hypoxia increases glucose concentrations in nondiabetic humans. We hypothesized plasma glucose would be increased from baseline following 3 h of intermittent hypoxia in healthy humans independent of any effect on insulin sensitivity. Eight (7M/1F, 21-34 years) healthy subjects completed two study visits randomized to 3 h of intermittent hypoxia or continuous normoxia, followed by an oral glucose tolerance test. Intermittent hypoxia consisted of 25 hypoxic events per hour where oxygen saturation (SpO) was significantly reduced (Normoxia: 97 ± 1%, Hypoxia: 90 ± 2%, P < 0.01). Venous plasma glucose concentrations were measured on both visits before and after the 3 h protocol. No changes in plasma glucose were observed from baseline after 3 h of continuous normoxia (5.1 ± 0.2 vs. 5.1 ± 0.1 mmol/L, P > 0.05). In contrast, circulating glucose concentrations were increased after 3 h of intermittent hypoxia when compared to baseline (5.0 ± 0.2 vs. 5.3 ± 0.2 mmol/L, P = 0.01). There were no detectable changes in insulin sensitivity following intermittent hypoxia when compared to continuous normoxia, as assessed by the oral glucose tolerance test (P > 0.05). Circulating glucose is increased after 3 h of intermittent hypoxia in healthy humans, independent of any lasting changes in insulin sensitivity. These novel findings could explain, in part, the high prevalence of diabetes in patients with sleep apnea and warrant future studies to identify underlying mechanisms.
睡眠呼吸暂停与糖尿病之间存在独立关联。动物模型表明，睡眠呼吸暂停导致的间歇性缺氧会引起葡萄糖代谢改变和空腹血糖升高。然而，急性暴露于间歇性缺氧是否会增加非糖尿病患者的血糖浓度尚不清楚。我们假设，健康人在间歇性缺氧3小时后，血浆葡萄糖会较基线水平升高，且与对胰岛素敏感性的任何影响无关。八名（7名男性/1名女性，21 - 34岁）健康受试者完成了两次研究访视，随机接受3小时的间歇性缺氧或持续常氧，随后进行口服葡萄糖耐量试验。间歇性缺氧包括每小时25次缺氧事件，在此期间血氧饱和度（SpO）显著降低（常氧：97±1%，缺氧：90±2%，P<0.01）。在3小时方案前后的两次访视中均测量静脉血浆葡萄糖浓度。持续常氧3小时后，血浆葡萄糖较基线水平无变化（5.1±0.2 vs. 5.1±0.1 mmol/L，P>0.05）。相比之下，间歇性缺氧3小时后，循环葡萄糖浓度较基线水平升高（5.0±0.2 vs. 5.3±0.2 mmol/L，P = 0.01）。通过口服葡萄糖耐量试验评估，与持续常氧相比，间歇性缺氧后胰岛素敏感性无明显变化（P>0.05）。健康人在间歇性缺氧3小时后，循环葡萄糖增加，且与胰岛素敏感性的任何持久变化无关。这些新发现可能部分解释了睡眠呼吸暂停患者中糖尿病的高患病率，并值得未来开展研究以确定潜在机制。
