Ren Hui-Zhu, Zheng Miao-Yan, Shan Chun-Yan, Yang Ju-Hong, Xu Yan-Guang, Yang Yan-Hui, Wang Ying, Chen Li-Ming, Chang Bao-Cheng
Department of Nephrology, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Key Laboratory of Hormone and Development (Ministry of Health), Metabolic Disease Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China.
Department of Nephrology, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Key Laboratory of Hormone and Development (Ministry of Health), Metabolic Disease Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China.
J Diabetes Complications. 2015 Jul;29(5):675-8. doi: 10.1016/j.jdiacomp.2015.03.016. Epub 2015 Apr 6.
To investigate the relationship between circadian blood pressure (BP) variability and function of islet α and β cell in type 2 diabetes (T2D) with dyssomnia.
Patients with T2D were divided into dyssomnia group and non-dyssomnia group by PSQI. OGTT, insulin and glucagon-releasing test were tested, and ambulatory BP was monitored for 24 hours to compare two groups with α and β cell, circadian BP variability and fasting and post-meal BP variability. The correlation and regression analysis were made between PSQI and other indicators.
In dyssomnia group, ① Glucagon, glucagon/insulin ratio and AUCG were significantly higher (P < 0.05). ② Fasting insulin (13.32 ± 4.54 mIU/L), AUCI (8.51 ± 0.54) and HOMA-IR (4.62 ± 1.11) were high (P < 0.05). But ISI (-4.27 ± 0.77) was low (P < 0.05). ③ Mean 24-hour and nighttime SBP and DBP, as well as their standard deviations and coefficients of variation, were all higher in the dyssomnia group (P < 0.05). Multiple stepwise regression analysis showed that PSQI score was positively related to AUCG, HOMA-IR, nighttime SBP, and negatively related to ISI and nocturnal BP fall (P < 0.05).
Dyssomnia may cause abnormal circadian BP variability through various mechanisms. Improving dyssomnia can help to better function the islet α and β cell and restore normal circadian BP variability.
探讨2型糖尿病（T2D）伴失眠患者昼夜血压（BP）变异性与胰岛α细胞和β细胞功能之间的关系。
采用匹兹堡睡眠质量指数（PSQI）将T2D患者分为失眠组和非失眠组。进行口服葡萄糖耐量试验（OGTT）、胰岛素和胰高血糖素释放试验，并监测24小时动态血压，以比较两组患者的α细胞和β细胞功能、昼夜血压变异性以及空腹和餐后血压变异性。对PSQI与其他指标进行相关性和回归分析。
在失眠组中，①胰高血糖素、胰高血糖素/胰岛素比值和曲线下面积（AUCG）显著升高（P<0.05）。②空腹胰岛素（13.32±4.54 mIU/L）、曲线下胰岛素分泌量（AUCI，8.51±0.54）和稳态模型胰岛素抵抗指数（HOMA-IR，4.62±1.11）较高（P<0.05）。但胰岛素敏感指数（ISI，-4.27±0.77）较低（P<0.05）。③失眠组24小时平均收缩压（SBP）和舒张压（DBP）、夜间SBP和DBP及其标准差和变异系数均较高（P< 0.05）。多元逐步回归分析显示，PSQI评分与AUCG、HOMA-IR、夜间SBP呈正相关，与ISI和夜间血压下降呈负相关（P<0.05）。
失眠可能通过多种机制导致昼夜血压变异性异常。改善失眠有助于胰岛α细胞和β细胞更好地发挥功能，并恢复正常的昼夜血压变异性。
