NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London, London, UK.
J Clin Sleep Med. 2011 Oct 15;7(5):486-92B. doi: 10.5664/JCSM.1314.
Understanding the etiologic mechanisms underlying impaired glucose tolerance in obstructive sleep apnea (OSA) would assist development of therapies against this comorbidity. We hypothesized that in patients with OSA impaired glucose tolerance (IGT) would be associated with elevated levels of hormones associated with appetite regulation (leptin, ghrelin, neuropeptide Y [NPY] and peptide tyrosine-tyrosine [PYY]).
We studied 68 OSA patients (mean AHI 22 events/h) and 37 age and weight matched healthy controls recruited by advertisement. All participants received a standardized evening meal, attended polysomnography and an oral glucose tolerance test (OGTT) on waking. Hormones were measured in blood taken before sleep (22:30) and at the start of the OGTT.
Impaired glucose tolerance was present in 54% of patients and 32% of controls (p = 0.05). The only differences between groups was that leptin was significantly higher at 22:30 in OSA patients compared to controls (9.6 ng/L vs 7.9 ng/L, p = 0.05). OSA patients had marginally elevated plasma NPY levels at 22:30 (56.6 [52, 67] pmol/L vs 51.1[47.3, 61] pmol/L; p = 0.04). No differences in ghrelin, PYY or NPY were observed between patients with IGT and those without. However OSA patients with IGT had significantly higher value of leptin at both 22:30 (10.9 [7.7, 15.9] ng/mL vs 7.4 [5.6, 12.3] ng/mL, p = 0.02) and 07:00 (11.6 [7.6, 16.2] ng/mL vs 6.9 [5.4, 12.6] ng/mL, p = 0.024) than those without. In multivariate analysis the only major association of leptin was body mass index.
Clinically significant abnormalities of appetite regulating hormones are not present in OSA. Appetite regulating hormones did not differ in OSA patients with and without impaired glucose tolerance.
了解阻塞性睡眠呼吸暂停(OSA)患者葡萄糖耐量受损的病因机制将有助于开发针对这种合并症的治疗方法。我们假设,在 OSA 患者中,葡萄糖耐量受损(IGT)与食欲调节激素(瘦素、胃饥饿素、神经肽 Y [NPY]和肽酪氨酸-酪氨酸 [PYY])水平升高有关。
我们研究了 68 例 OSA 患者(平均 AHI 为 22 次/小时)和 37 例年龄和体重匹配的健康对照组,通过广告招募。所有参与者均接受标准的晚餐,在醒来后进行多导睡眠图和口服葡萄糖耐量试验(OGTT)。在睡前(22:30)和 OGTT 开始时采集血液以测量激素。
54%的患者和 32%的对照组存在葡萄糖耐量受损(p=0.05)。两组之间唯一的差异是 OSA 患者的瘦素在 22:30 时明显高于对照组(9.6ng/L 与 7.9ng/L,p=0.05)。OSA 患者的血浆 NPY 水平在 22:30 时略有升高(56.6[52,67]pmol/L 与 51.1[47.3,61]pmol/L;p=0.04)。IGT 和非 IGT 患者之间的胃饥饿素、PYY 或 NPY 无差异。然而,IGT 的 OSA 患者在 22:30(10.9[7.7,15.9]ng/mL 与 7.4[5.6,12.3]ng/mL,p=0.02)和 07:00(11.6[7.6,16.2]ng/mL 与 6.9[5.4,12.6]ng/mL,p=0.024)时的瘦素值明显更高。多元分析显示,瘦素的唯一主要关联是体重指数。
OSA 患者不存在明显的食欲调节激素异常。OSA 患者中,葡萄糖耐量受损和无葡萄糖耐量受损患者的食欲调节激素无差异。