中文摘要：

目的 探讨2型糖尿病患者睡眠障碍与黎明现象的关系.方法 应用匹兹堡睡眠质量指数将2011年7月至2014年7月天津医科大学代谢病医院收治的316例行动态血糖监测、资料完整的2型糖尿病患者分为无睡眠障碍组（186例）和睡眠障碍组（130例）,测定肝肾功能、血脂、糖化血红蛋白（HbA1c）、果糖胺等生化指标,行口服葡萄糖耐量试验及胰岛素、胰高糖素释放试验,比较两组血糖水平、空腹和糖负荷后胰岛α和β细胞功能变化,对睡眠障碍行相关及回归分析.结果 睡眠障碍组HbA1c、果糖胺、空腹血糖与夜间最低点血糖净增值、早餐后与早餐前血糖净增值、24 h平均血糖、空腹胰岛素、稳态模型-胰岛素抵抗指数（HOMA-IR）、胰岛素曲线下面积均显著高于无睡眠障碍组[（8.2±2.0）％比（7.4±1.7）％,（0.33±0.10）比（0.29 ±0.07） mmol/L,（1.511 ±0.294）比（0.889±0.233） mmol/L,（2.144±0.400）比（1.522±0.378） mmol/L,（9.917±1.800）比（8.694±1.622） mmol/L,（13.49±4.68）比（12.16±4.56） mU/L,4.98±0.90比3.82±0.82,8.47 ±0.59比8.25 ±0.54]（均P＜0.05）.睡眠障碍组胰岛素敏感指数显著低于无睡眠障碍组（-4.28 ±0.62比-4.03 ±0.52）,各时间点胰高糖素水平及胰高糖素曲线下面积均显著高于无睡眠障碍组,0、30、180 min胰高糖素/胰岛素比值及胰高糖素/血糖比值也均显著高于无睡眠障碍组（均P＜0.05）.睡眠障碍与HOMA-IR、胰高糖素/胰岛素比值、空腹血糖与夜间最低点血糖净增值、黎明现象均呈正相关,与胰岛素敏感指数呈负相关（均P＜0.05）.结论 睡眠障碍与黎明现象相关,改善睡眠障碍可能有助于改善黎明现象,从而优化整体血糖控制.

英文摘要：

Objective To explore the association between sleep disorders and dawn phenomenon in patients with type 2 diabetes mellitus （T2DM）.Methods From July 2011 to July 2014 at Metabolic Disease Hospital,Tianjin Medical University,316 T2DM patients on continuous glucose monitoring were divided into two groups according to the Pittsburgh Sleep Quality Index,i.e.those without sleep disorders （n =186） and those with sleep disorders （n =130）.Biochemical parameters including hepatorenal functions,blood lipids,glycosylated hemoglobin （HbA1c） and fructosamine were detected.Oral glucose tolerance test,insulin releasing test and glucagon releasing test were performed to detect the inter-group differences of glucose concentration and α-cell and β-cell functions after fasting and glucose loading.And the correlation and regression analyses were performed between sleep disorders and other parameters.Results The level of HbA1c,fructosamine,increment of fasting glucose and nocturnal nadir glucose,glucose increment before and after breakfast,24 h mean glucose,fasting insulin,homeostasis model assessment of insulin resistance index （HOMA-IR） and area under curve of insulin were significantly higher in patients with sleep disorders than those without sleep disorders （8.2% ±2.0% vs 7.4% ± 1.7%,（0.33 ±0.10） vs （0.29 ±0.07） mmol/L,（1.511 ±0.294） vs （0.889 ±0.233） mmol/L,（2.144 ±0.400） vs （1.522±0.378） mmol/L,（9.917±1.800） vs （8.694±1.622） mmol/L,（13.49±4.68） vs （12.16±4.56） mU/L,4.98 ± 0.90 vs 3.82 ± 0.82,（8.47 ±0.59） vs （8.25 ±0.54）,all P〈0.05）.Insulin sensitivity index was lower in patients with sleep disorders than that in those without sleep disorders （-4.28 ± 0.62 vs-4.03 ± 0.52,P 〈 0.05）.The level of glucagon at each timepoint and area-undercurve of glucagon were significantly higher in patients with sleep disorders than those without sleep disorders.The levels of 0,30,180 min glucagon/insulin ratio and glucagon/glucose ratio were signif