Karamullina R A, Ismailova S M, Pesheva E D, Poluboyarinova I V, Poluektov M G, Fadeev V V
I.M. Sechenov First Moscow State Medical University (Sechenovskiy University).
Probl Endokrinol (Mosk). 2025 May 20;71(2):45-54. doi: 10.14341/probl13318.
Usually, a hypoglycemic episode occurs due to inadequacy of the administered insulin dose in accordance with the current physiological situation. Activated systems aimed at increasing blood glucose levels serve as precursors of hypoglycemia and markers of the severity of hyperinsulinemia. Therefore, determining their components can serve as a more subtle and sensitive approach to assessing the physiological appropriateness of different insulin therapy options.
To investigate the markers (biochemical, clinical, and morphological) and the degree of activation of the stress system preceding the development of hypoglycemic episodes in patients with type 1 diabetes (T1D) undergoing insulin therapy.
A cross-sectional observational clinical study was conducted involving 74 patients with type 1 diabetes (T1D). All patients underwent examination, which included assessment of the history of hypoglycemic episodes, quality of life using the SF-36 questionnaire, levels of adrenocorticotropic hormone (ACTH), insulin-like growth factor-1 (IGF-1), cortisol, C-reactive protein (CRP), coagulation profile, and 24-hour urinary cortisol excretion. Evaluation of patients' sleep characteristics was performed based on the results of completed questionnaires: Sleep Questionnaire and Epworth Sleepiness Scale. Patients underwent overnight polysomnography (PSG) with interpretation according to the AASM 2012 standards.
Patients with a higher frequency of hypoglycemic episodes showed a decrease in IGF-1 levels at all stages (140 [123:162]; 98 [93:121], p=0.005), worse quality of life scores across all domains of the SF-36 questionnaire (95 [88:100]; 84 [77:92], p=0.001). As the frequency of hypoglycemic episodes increased, polysomnography data revealed an increase in the number of awakenings lasting more than 3 minutes (2 [1:3]; 3 [2:4]; p=0.03), increased time spent in bed (493.1 [463.95:513.4]; 536.2 [511.6:551]; p=0.03), increased sleep duration (437.5 [430.05:468]; 489 [471.5:519], p=0.006), and in creased total sleep time (382.5 [321.75:422]; 439 [409.5:486], p=0.008).
An increase in the frequency of hypoglycemic episodes should be accompanied by activation of the stress response system; however, repeated episodes of hypoglycemia lead to depletion of the stress response system, as evidenced by a decrease in the level of IGF-1 in patients with frequent hypoglycemic episodes. Hypoglycemic episodes occurring not only during night time but also at other times disrupt the sleep structure by increasing the frequency of nocturnal awaken ings.
通常,低血糖发作是由于所给予的胰岛素剂量与当前生理状况不匹配所致。旨在提高血糖水平的激活系统是低血糖的先兆以及高胰岛素血症严重程度的标志物。因此,确定其组成成分可作为一种更精细、敏感的方法,用于评估不同胰岛素治疗方案的生理适宜性。
研究接受胰岛素治疗的1型糖尿病(T1D)患者在低血糖发作前应激系统的标志物(生化、临床和形态学)及激活程度。
进行了一项横断面观察性临床研究,纳入74例1型糖尿病(T1D)患者。所有患者均接受检查,包括评估低血糖发作史、使用SF-36问卷评估生活质量、促肾上腺皮质激素(ACTH)、胰岛素样生长因子-1(IGF-1)、皮质醇、C反应蛋白(CRP)水平、凝血指标以及24小时尿皮质醇排泄量。根据完成的问卷结果评估患者的睡眠特征:睡眠问卷和爱泼华嗜睡量表。患者接受整夜多导睡眠图(PSG)检查,并根据2012年美国睡眠医学学会(AASM)标准进行解读。
低血糖发作频率较高的患者在各个阶段IGF-1水平均降低(140[123:162];98[93:121],p = 0.005),SF-36问卷所有领域的生活质量评分更差(95[88:100];84[77:92],p = 0.001)。随着低血糖发作频率增加,多导睡眠图数据显示持续超过3分钟的觉醒次数增加(2[1:3];3[2:4];p = 0.03),卧床时间增加(493.1[463.95:513.4];536.2[511.6:551];p = 0.03),睡眠时间增加(437.5[430.05:468];489[471.5:519];p = 0.006),总睡眠时间增加(382.5[321.75:422];439[409.5:486];p = 0.008)。
低血糖发作频率增加应伴有应激反应系统的激活;然而,反复低血糖发作会导致应激反应系统耗竭,频繁低血糖发作患者的IGF-1水平降低即证明了这一点。不仅夜间而且其他时间发生的低血糖发作会通过增加夜间觉醒频率扰乱睡眠结构。