Article(id=1322167925428040596, tenantId=1146029695717560320, journalId=1220038315760373764, issueId=1322167871413796899, articleNumber=null, orderNo=null, doi=10.12102/j.issn.1009-6493.2026.03.020, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1740844800000, receivedDateStr=2025-03-02, revisedDate=1762617600000, revisedDateStr=2025-11-09, acceptedDate=null, acceptedDateStr=null, onlineDate=1793158998113, onlineDateStr=2026-10-28, pubDate=1770652800000, pubDateStr=2026-02-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793158998113, onlineIssueDateStr=2026-10-28, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793158998113, creator=13701087609, updateTime=1793158998113, updator=13701087609, issue=Issue{id=1322167871413796899, tenantId=1146029695717560320, journalId=1220038315760373764, year='2026', volume='40', issue='3', pageStart='353', pageEnd='528', issueExtLink='null', onlineDate='null', pubDate='1770652800000', pubDateStr='2026-02-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1793158985236, creator='13701087609', updateTime=1793158985236, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=490, endPage=496, ext={EN=ArticleExt(id=1322167925662921621, articleId=1322167925428040596, tenantId=1146029695717560320, journalId=1220038315760373764, language=EN, title=Research progress on the bidirectional association mechanism between glycemic variability and sleep quality and multidimensional nursing interventions, columnId=1220689485315101342, journalTitle=Chinese Nursing Research, columnName=Review Articles, runingTitle=null, highlight=null, articleAbstract=

This article reviewed the interaction mechanism between sleep quality and glycemic variability,as well as the application of multidimensional nursing intervention strategies,so as to provide reference for the development of precision nursing practice.

, authors=Yuxin ZHONG, Zhenzhen XIONG, authorsList=Yuxin ZHONG, Zhenzhen XIONG, authorCompany=null, correspAuthors=Zhenzhen XIONG, authorNote=null, correspAuthorsNote=
XIONG Zhenzhen, E-mail:
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综述睡眠质量与血糖变异性之间的交互机制及多维护理干预策略的应用,以期为精准护理实践的发展提供参考。

, authors=钟雨欣, 熊真真*, *, authorsList=钟雨欣, 熊真真, authorCompany=null, correspAuthors=熊真真, authorNote=

钟雨欣,护师,硕士研究生在读

, correspAuthorsNote=
熊真真,E-mail:
XIONG Zhenzhen, E-mail:
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钟雨欣,护师,硕士研究生在读

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钟雨欣,护师,硕士研究生在读

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血糖变异性与睡眠质量双向关联机制及多维护理干预的研究进展
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钟雨欣 , 熊真真 *, *
护理研究 | 科研综述 2026,40(3): 490-496
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护理研究 |科研综述 2026 , 40 (3) : 490 -496
血糖变异性与睡眠质量双向关联机制及多维护理干预的研究进展
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钟雨欣, 熊真真*, *
作者信息
  • 1成都医学院护理学院,四川 610036
通讯作者:
熊真真,E-mail:
XIONG Zhenzhen, E-mail:
作者简介:

钟雨欣,护师,硕士研究生在读

Research progress on the bidirectional association mechanism between glycemic variability and sleep quality and multidimensional nursing interventions
Yuxin ZHONG, Zhenzhen XIONG
Affiliations
  • 1College of Nursing, Chengdu Medical College, Sichuan 610036 China
  • Corresponding Author:
    XIONG Zhenzhen, E-mail:
出版时间: 2026-02-10 doi: 10.12102/j.issn.1009-6493.2026.03.020
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综述睡眠质量与血糖变异性之间的交互机制及多维护理干预策略的应用,以期为精准护理实践的发展提供参考。

血糖变异性  /  睡眠质量  /  多维护理  /  干预策略  /  综述

This article reviewed the interaction mechanism between sleep quality and glycemic variability,as well as the application of multidimensional nursing intervention strategies,so as to provide reference for the development of precision nursing practice.

glycemic variability  /  sleep quality  /  multidimensional nursing  /  intervention strategies  /  review
钟雨欣, 熊真真. 血糖变异性与睡眠质量双向关联机制及多维护理干预的研究进展. 护理研究, 2026 , 40 (3) : 490 -496 . DOI: 10.12102/j.issn.1009-6493.2026.03.020
Yuxin ZHONG, Zhenzhen XIONG. Research progress on the bidirectional association mechanism between glycemic variability and sleep quality and multidimensional nursing interventions[J]. Chinese Nursing Research, 2026 , 40 (3) : 490 -496 . DOI: 10.12102/j.issn.1009-6493.2026.03.020
目前,全球糖尿病与睡眠障碍的流行趋势已构成重大公共卫生挑战。世界卫生组织(WHO)及Lecent报告显示,普通人群中约40%合并睡眠障碍,糖尿病病人中睡眠障碍患病率显著升高,这一双重疾病负担提示,二者间交互作用或是代谢紊乱相关疾病的潜在靶点[1-2]。血糖变异性(glycemic variability,GV)是指在某一特定时间范围内,血糖水平所呈现的波动状态,可通过量化血糖峰谷变化更精准地反映糖尿病管理质量。研究表明,血糖变异性能够独立于糖化血红蛋白(HbA1c)预测糖尿病微血管与大血管并发症的发生风险,可能是心血管疾病风险的独立风险因素[3-4]。血糖变异性波动幅度越大,糖尿病慢性并发症发生风险越高,病人更易发生心血管疾病、视网膜疾病和肾脏病等并发症[5-6]。然而,临床实践中仍以糖化血红蛋白为主要指标,针对血糖变异性的系统性管理策略及调控路径尚存在不足。研究显示,通过监测睡眠效率(sleep efficiency,SE)能够预测个体内较高的血糖变异性,长期的睡眠不连续性或中断会加剧血糖的不稳定性,从而增加糖尿病病人并发症的发生风险[7]。据报道,睡眠效率<80%的人群糖尿病患病率显著高于睡眠效率≥85%的人群,且睡眠效率降低与血糖控制恶化相关,通过优化睡眠效率并维持夜间正常血糖范围,可能是打破“睡眠紊乱-血糖失衡”恶性循环的关键机制[7-8]。但目前研究多侧重血糖变异性与睡眠质量的单一维度关联分析,对双向机制及多维护理干预策略的探索不足。本研究就血糖变异性和睡眠障碍的交互机制,多维护理干预措施在改善睡眠质量及调控血糖变异性中的作用进行综述,旨在为制定慢性病管理相关的综合护理策略提供参考。
研究表明,1型糖尿病(type 1 diabetes,T1DM)或2型糖尿病(type 2 diabetes,T2DM)病人的睡眠时间或结构与血糖变异性存在显著相关性,优化睡眠结构可以有效改善血糖控制水平[9]。长期睡眠限制(chronic sleep restriction,CSR)或长期睡眠不足(long-term sleep deprivation,SD)是代谢性疾病的重要危险因素,其具体效应机制尚不清楚,下丘脑-垂体-肾上腺轴可能是重要中介[10]。皮质醇是下丘脑-垂体-肾上腺轴的终端激素,其分泌受到睡眠模式的影响[11]。研究显示,长期睡眠限制可导致皮质醇昼夜节律相位偏移,峰值水平升高,且夜间皮质醇分泌抑制效应减弱,从而通过增加肝糖原分解、增强糖异生、降低胰岛素敏感性等机制加剧血糖波动[12-13]。研究发现,长期睡眠限制能够显著降低人体内瘦素水平,胃饥饿素升高,相比于24 h急性睡眠剥夺,胰岛素水平及胰岛素敏感性变化更明显[14]。下丘脑-垂体-肾上腺轴功能失调主要通过促肾上腺皮质激素(adrenocorticotropic hormone,ACTH)反馈机制和促肾上腺皮质激素释放激素(corticotropin releasing hormone,CRH)分泌异常等途径,干扰皮质醇的正常分泌节律[15]。长期睡眠限制可造成促肾上腺皮质激素对促肾上腺皮质激素释放激素的总体反应降低27%,而皮质醇反应降低21%[16]。上述研究说明,长期睡眠限制/长期睡眠不足能够通过神经内分泌系统降低胰岛素敏感性、增强胰岛素抵抗,从而导致血糖变异性增大。下丘脑-垂体-肾上腺轴活动失调造成皮质醇昼夜节律异常可能是其核心机制,通过缓解长期睡眠限制/长期睡眠不足能够改善糖代谢异常及胰岛素抵抗[17]。
生物钟基因在下丘脑-垂体-肾上腺轴的节律性调节中具有关键作用,其通过调节下丘脑促肾上腺皮质激素释放激素的分泌,影响下丘脑-垂体-肾上腺轴的活动,从而调控皮质醇的分泌节律[18]。研究显示,皮质醇可通过驱动时钟昼夜节律调节器(clock circadian regulator,CLOCK)和周期昼夜节律时钟(period circadian clock 1,PER)基因家族的昼夜节律或超昼夜节律突变转录活动,在机体代谢、应激及免疫等疾病中起重要作用[19]。糖皮质激素受体(glucocorticoid receptor,GR)是人类代谢节律性的主要中枢神经系统决定因素,其周期性的维持通过时钟昼夜节律调节器基因对糖皮质激素受体的乙酰化和糖皮质激素受体Y1、糖皮质激素受体Y2对糖皮质激素受体表达的节律性抑制调节[19]。时钟昼夜节律调节器-Bmal异源二聚体能够通过糖皮质激素受体的乙酰化调节外周组织对糖皮质激素的反应,从而拮抗昼夜波动的循环皮质醇的生物作用[20]。另有研究表明,N6-甲基腺苷(N6-methyladenosine,m6A)RNA甲基化也参与了昼夜节律调控,长期高皮质醇暴露可导致下丘脑和垂体中时钟基因的昼夜节律受到不同程度的干扰,下丘脑m6A的摆动模式与促肾上腺皮质激素释放激素mRNA相反[21]。进一步对促肾上腺皮质激素释放激素mRNA的3'UTR特定位点m6A分析证实,促肾上腺皮质激素释放激素mRNA 3'UTR上较高的m6A与夜间较低的促肾上腺皮质激素释放激素mRNA相吻合,说明RNA m6A修饰参与了下丘脑的昼夜节律调节[21]。因此,生物钟基因和表观遗传修饰是昼夜节律的重要调节机制。
Zhang等[22]研究表明,睡眠障碍能够通过激活炎症与氧化应激通路,导致免疫细胞活化、线粒体功能障碍及抗氧化防御系统损伤,从而影响糖代谢平衡,加剧血糖波动。在不缩短睡眠时间的情况下,碎片化睡眠(sleep fragmentation,SF)可诱导内脏脂肪组织(visceral adipose tissue,VAT)的时间依赖性胰岛素抵抗,结果显示,碎片化睡眠上调了内脏脂肪组织中的氧化应激通路,并伴随M1巨噬细胞极化现象。说明碎片化睡眠可能通过激活炎症和氧化应激,从而诱导胰岛素抵抗,为糖尿病的综合治疗提供了新思路,M1巨噬细胞极化可能在此过程中发挥了关键作用。长期睡眠不足可导致认知和记忆丧失,并加重神经退行性病变程度,小胶质细胞介导的慢性炎症在其中起到重要作用[23]。烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD+)是一种氧化还原辅酶,在小胶质细胞中具有抗炎和保护线粒体的功能,通过睡眠限制方式干预还原型辅酶Ⅱ(NADPH)氧化酶2(Nox2)缺乏小鼠3 d至3周后表现出胰岛素抵抗的时间依赖性[22-23]。Chen等[23]体内试验证实,补充烟酰胺腺嘌呤二核苷酸可以抑制体内促炎细胞因子的表达,从而改善睡眠质量,缓解长期睡眠限制/长期睡眠不足造成的神经系统损伤,进一步细胞实验显示,烟酰胺腺嘌呤二核苷酸可抑制活性氧(ROS)的产生,并促使M1向M2表型转化,而cGAS-STING/NF-κB信号通路可能是小胶质细胞促炎的关键通路。上述研究提示,通过补充烟酰胺腺嘌呤二核苷酸调节小胶质细胞功能缓解长期睡眠限制/长期睡眠不足,从而改善糖代谢和胰岛素抵抗,可能是降低血糖变异性的潜在靶点,人类中枢神经系统相关巨噬细胞的活化以及外周巨噬细胞极化的状态可能是改善胰岛素抵抗的直接或间接因素,但其具体机制仍未明确。
睡眠质量或睡眠模式改变是糖尿病病人常见的临床特征之一,通常与血糖调控呈负相关,但有关睡眠模式与糖尿病的具体关系仍未明确[24]。慢波睡眠(slow wave sleep,SWS)在维持正常血糖稳态和胰岛素分泌方面发挥着关键作用,慢波睡眠减少是糖尿病发病风险的显著危险因素[24]。在不缩短总睡眠时间的情况下,选择性抑制睡眠呼吸暂停会导致胰岛素抵抗显著增强、糖耐量降低以及糖尿病风险升高[24]。因此,了解糖尿病病人睡眠模式的变化对糖尿病发病风险及血糖控制的影响,对于降低糖尿病相关疾病负担有重要价值。Botella-Serrano等[25]研究显示,不同睡眠模式集群表现出不同的血糖特征,1型糖尿病病人的主观和客观睡眠质量较差,且睡眠质量与夜间血糖变异性有关,改善1型糖尿病病人的睡眠质量可以改善血糖控制质量。Zhang等[26]通过认知行为疗法(cognitive behavioral therapy,CBT)对1 033例2型糖尿病伴睡眠质量差的病人进行了干预治疗,并以糖化血红蛋白和匹兹堡睡眠质量指数(Pittsburgh Sleep Quality Index,PSQI)作为疗效评估指标。结果显示,认知行为疗法联合常规护理组与常规护理组相比,在2、6、12个月时PSQI得分分别比对照组低0.64、0.50、0.90分。在6、12个月时,认知行为疗法组的糖化血红蛋白分别比对照组低0.17%和0.43%。12个月时,PSQI得分与糖化血红蛋白相关(t=7.02,P<0.01)。提示睡眠质量与血糖控制之间存在潜在联系,改善睡眠质量是调节2型糖尿病病人血糖波动水平的重要干预措施,其疗效具有时间依赖性,常规护理联合多种辅助治疗方案更有利于糖尿病病人的血糖控制。
研究表明,血糖变异性与睡眠质量之间存在动态交互关系,这种关系在1型糖尿病、2型糖尿病、妊娠糖尿病及糖尿病前期病人中更为明显[25-27]。Martyn-Nemeth等[27]对48例1型糖尿病病人的睡眠质量与糖化血红蛋白和血糖变异性间的关系进行分析,结果显示,1型糖尿病病人血糖波动与睡眠效率降低存在正相关关系,48%的1型糖尿病病人伴有睡眠质量差,且夜间血糖变异性明显增加。血糖骤降会触发觉醒,1型糖尿病病人夜间低血糖事件发生时睡眠结构会受到明显干扰,主要表现为快速眼动睡眠时间缩短和非快速眼动睡眠分布不均[27]。此外,高频小幅波动与觉醒指数呈现J型关联,表明微小的血糖波动也可能影响夜间觉醒的频率[28]。在2型糖尿病病人中普遍存在血糖变异性与睡眠障碍的疾病共病现象,血糖变异性增加可能通过影响神经内分泌系统,进而干扰睡眠质量[29]。Hwang等[30]研究显示,接受糖尿病管理的病人睡眠质量差的报告显著降低,出现片段化睡眠、夜尿、睡眠疼痛和入睡困难等症状相对较少。上述研究提示,睡眠质量差与血糖控制在一定范围内、血糖变异性幅度较大有关,控制血糖波动是改善糖尿病病人睡眠质量的有效干预目标。然而,有关血糖波动对睡眠质量影响的临床证据逐渐增多,但其具体机制研究相对较少。
下丘脑是调节睡眠-觉醒周期的关键区域,其外侧的食欲素(orexin)神经元在促进觉醒和维持睡眠稳定性方面发挥重要作用。研究表明,食欲素神经元对血糖变化敏感,其活性受葡萄糖波动调控,食欲素水平降低与睡眠障碍具有显著相关性,提示食欲素神经元可能在介导代谢与睡眠的互作关系中起关键作用[31-32]。长期的高血糖可能通过氧化应激和线粒体功能障碍,诱导下丘脑食欲素神经元凋亡,从而导致睡眠-觉醒周期紊乱,影响睡眠质量[32]。褪黑素是调节睡眠的重要激素,其缺乏不仅影响睡眠的初始和维持,还可能与认知功能下降和情绪障碍相关联[33]。在高血糖状态下,2型糖尿病病人胰岛素抵抗加重会导致褪黑素的合成受损,形成血糖波动与睡眠障碍之间的双向反馈关系[34]。因此,改善胰岛素敏感性可能有助于恢复褪黑素的正常分泌,从而改善睡眠质量。长期高血糖可导致三羧酸循环、氨基酸代谢和脂质代谢等多个途径的紊乱,这些代谢变化与周围和中枢神经系统的损伤密切相关[35-36]。高血糖状态下,游离脂肪酸水平升高是影响睡眠调控网络的因素之一。过高的游离脂肪酸通过诱导氧化应激和炎症反应破坏血脑屏障紧密连接蛋白ZO-1,导致血脑屏障通透性增加,从而促进血浆游离色氨酸进入脑内,导致5-羟色胺合成增加以及5-羟色胺能神经元功能紊乱[37-38]。以上研究表明,血糖的波动不仅影响身体的代谢状态,还对中枢神经系统的功能产生显著影响,血糖波动、代谢紊乱与睡眠障碍之间的复杂关系尚未阐明,针对代谢物异常的干预可能为改善糖尿病病人睡眠障碍提供了新的治疗思路。
单磷酸腺苷活化蛋白激酶(AMP-activated protein kinase,AMPK)和哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)通路在能量代谢和细胞生长中具有至关重要的作用。单磷酸腺苷(AMP)活化蛋白激酶在能量或营养缺乏时被激活,抑制细胞生长,而哺乳动物雷帕霉素靶蛋白则在营养充足时被激活,促进细胞生长,二者在细胞营养感知和生长控制中存在复杂的交互调节机制[39]。研究显示,细胞内单磷酸腺苷/三磷酸腺苷(ATP)比例控制单磷酸腺苷活化蛋白激酶的活性,在调节睡眠/觉醒周期和睡眠稳态方面发挥功能[40-41]。Chikahisa等[42]发现,体外注射单磷酸腺苷活化蛋白激酶抑制剂5-氨基咪唑-4-羧基酰胺核苷(5-aminoimidazole-4-carboxamide riboside,AICAR),能够增强非快速眼动睡眠的睡眠慢波活动(slow-wave sleep,SWS)。6 h睡眠剥夺后单磷酸腺苷活化蛋白激酶上游激酶钙离子(Ca2+)/钙调蛋白依赖性蛋白激酶β(Ca2+/calmodulin-dependent protein kinase kinase beta,CaMKK2)mRNA的表达增加,同时伴有三磷酸腺苷降低,而单磷酸腺苷活化蛋白激酶下游信号分子肉碱棕榈酰基转移酶1(carnitine palmitoyltransferase 1,CPT1)的mRNA表达在睡眠剥夺恢复期增加[42]。上述研究提示,单磷酸腺苷活化蛋白激酶作为能量感知器,能够感知细胞内的能量状态,从而参与睡眠深度和睡眠平衡的调节,长时间的清醒可以通过增加单磷酸腺苷/三磷酸腺苷比例和/或钙调蛋白依赖性蛋白激酶β表达增强中枢单磷酸腺苷活化蛋白激酶的活性,从而导致非快速眼动睡眠时睡眠慢波活动的增强。
哺乳动物雷帕霉素靶蛋白主要通过哺乳动物雷帕霉素靶蛋白复合物1(mTORC1)和哺乳动物雷帕霉素靶蛋白复合物2(mTORC2)复合体形式参与调节神经元的突触传递。mTORC1在突触后传递的调节中发挥作用,而哺乳动物雷帕霉素靶蛋白复合物2则影响突触前信号传导,这些信号途径的改变是哺乳动物雷帕霉素靶蛋白活性波动导致神经疾病的主要机制之一[39]。单磷酸腺苷活化蛋白激酶与哺乳动物雷帕霉素靶蛋白在功能上存在相互拮抗效应,单磷酸腺苷活化蛋白激酶通过磷酸化异源三聚体TSC2和RAPTOR双重机制抑制哺乳动物雷帕霉素靶蛋白复合物1 [39]。长期睡眠剥夺可能通过脑内前列腺素D2(PGD2)积累触发外周免疫反应,从而导致细胞因子风暴,间接影响单磷酸腺苷活化蛋白激酶/哺乳动物雷帕霉素靶蛋白信号通路[39,43]。研究显示,单磷酸腺苷活化蛋白激酶与昼夜节律有关,其可以通过Cry1 Ser 71位点的磷酸化调节核心时钟成分Cry1的稳定性,从而刺激F-box蛋白质Fbxl3的直接结合Cry1[44]。此外,单磷酸腺苷活化蛋白激酶参与对肌肉和脂肪中葡萄糖摄取、脂肪酸和甾醇合成的速率限制性步骤以及脂肪酶等的直接影响控制,其在肝脏中通过磷酸化和抑制cAMP反应元件结合蛋白调控的转录共激活因子2(CRCT2)和类Ⅱa HDACs负性调节糖异生[44]。因此,调节单磷酸腺苷活化蛋白激酶/mTOR通路的活性可能成为改善睡眠质量和代谢健康的潜在策略。
沉默信息调节因子2相关酶1(sirtuin 1,SIRT1)是一种依赖烟酰胺腺嘌呤二核苷酸的组蛋白组乙酰化酶,在Sirtuins家族成员中研究最为广泛,具有抗氧化、调节线粒体功能及保护神经等作用。在糖尿病疾病中,沉默信息调节因子2相关酶1的表达和活性常受到抑制,这与线粒体功能的损害密切相关。研究显示,上调沉默信息调节因子2相关酶1能显著抑制线粒体裂变,抑制过氧化物酶体增殖激活受体-γ辅激活因子-1α(PGC-1α)会减弱沉默信息调节因子2相关酶1对动力蛋白相关蛋白1(dynamin-related protein 1,DRP1)、线粒体裂变因子(mitochondrial fission factor,MFF)和线粒体裂变蛋白(mitochondrial fission 1,FIS1)以及线粒体裂变表达的积极影响,提示沉默信息调节因子2相关酶1通过过氧化物酶体增殖激活受体-γ辅激活因子-1α-动力蛋白相关蛋白1/线粒体裂变蛋白/线粒体裂变因子信号通路调节线粒体分裂,改善线粒体功能障碍,这可能与代谢紊乱中的线粒体动态平衡直接相关[45]。高糖环境下,沉默信息调节因子2相关酶1的激活减少了细胞氧化应激及炎症因子的释放,从而促进神经细胞的存活,提高神经传导速度[46]。Zhao等[47]研究发现,烟酰胺腺嘌呤二核苷酸能够通过沉默信息调节因子2相关酶1/过氧化物酶体增殖激活受体-γ辅激活因子-1α轴减少活性氧生成,调控线粒体生物合成及其抗氧化能力,从而抑制神经炎症,为代谢-睡眠关联提供了分子干预证据。综上所述,针对单磷酸腺苷活化蛋白激酶/mTOR通路和沉默信息调节因子2相关酶1/过氧化物酶体增殖激活受体-γ辅激活因子-1α轴的干预可能为改善血糖波动和睡眠障碍提供新的治疗思路。
多维护理干预策略是针对改善睡眠质量与血糖变异性之间的双向关系而提出的一系列综合性措施,主要包括生理维度、心理维度、行为-社会维度,旨在构建多维度综合护理策略,从而促进血糖控制。
睡眠质量与血糖变异性存在显著的相互影响关系,良好的睡眠卫生习惯能够显著提高睡眠质量,降低血糖变异性。研究显示,睡眠质量更稳定的人从一夜高质量睡眠中获益更多,较差的平均睡眠质量与较高的血糖风险有关,睡眠质量不一致性和每日偏差相互影响,可预测较高的血糖值[48]。1型糖尿病/2型糖尿病病人良好、稳定的睡眠质量均可减少代谢相关自我调节失败及高血糖风险,从而有利于糖尿病管理[48-49]。Tsereteli等[50]研究发现,睡眠模式与次日餐后血糖控制间存在显著相关性,睡眠持续时间、睡眠效果是人群餐后血糖控制的重要决定因素。孟意琳等[51]临床对照试验显示,采用睡眠健康管理系统(含规律作息、环境优化等干预)的糖尿病病人,PQSI评分降低30%,血糖波动标准差减少0.8 mmol/L,证实睡眠卫生管理对血糖稳定性的改善。因此,睡眠作为一种可调节的非药物治疗目标,能够优化人体代谢健康的调节,规律的作息习惯能够有效降低血糖变异性。
心理因素在糖尿病的管理中发挥着重要作用,借助正念减压(mindfulness-based stress reduction,MBSR)及病人决策支持工具,能够显著增强自我管理能力。Fisher等[52]研究显示,通过正念减压平均干预4.3个月后,能够显著减轻焦虑和抑郁症状,表明正念减压可能是改善糖尿病病人心理健康状况的一种有效疗法。Ni等[53]研究发现,糖尿病病人接受正念减压治疗后,抑郁得分、生活质量量表的心理维度得分及糖化血红蛋白均降低,随访6个月后糖化血红蛋白继续降低。上述研究表明,通过心理层面的干预措施可以有效促进病人的心理健康,从而改善其糖尿病管理效果。
行为因素是糖尿病管理的核心要素,生活方式改变以及家庭和社区支持作用能够显著提高糖尿病病人的自我管理能力和生活质量[54]。协助病人制定糖尿病社区护理中“医院-社区-家庭”三位一体支持网络及个性化健康管理档案,为病人提供全方位服务,可帮助提高病人的药物依从性,改善血糖波动,降低较大血糖变异性[55]。参与社区健康教育活动的病人在饮食控制和运动参与方面表现得更加积极,这直接影响了病人血糖的控制。姚裕忠等[56]通过“全专精准管理”的糖尿病“1358模式”对社区糖尿病病人进行干预管理,结果显示,干预病人空腹血糖达标率、糖化血红蛋白达标率等均高于对照组,且能够增强糖尿病病人的健康信念,规范血糖监测行为。因此,通过整合家庭和社区资源,构建个性化支持网络,可以为糖尿病病人提供更为全面的照护,帮助病人更好地应对疾病相关的挑战。
睡眠质量与血糖变异性之间存在复杂的双向关联机制,良好的睡眠质量可显著降低血糖波动,高血糖会反馈性地影响睡眠的质量和结构,为糖尿病管理提供了新的思路。在临床护理实践中,必须将睡眠管理与血糖控制相结合,主动纳入睡眠干预的内容,如认知行为疗法、正念减压和放松训练等方法,以提升病人的睡眠质量,实现更优的疗效。有效的干预措施应包括多方面的管理策略,行为干预、认知行为疗法和药物治疗等,都在改善睡眠质量和血糖控制方面显示出良好的效果。不同病人在睡眠与血糖管理上的需求和反应存在显著差异,通过对病人的生活方式、心理状态及病情进展进行全面评估,进而制定多维度干预策略及个性化的管理方案,能够更好地提高糖尿病的管理及治疗效果。未来的研究应致力于了解不同个体在睡眠与血糖控制方面的生理差异,从而为病人制定个性化管理方案。

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doi: 10.12102/j.issn.1009-6493.2026.03.020
  • 接收时间:2025-03-02
  • 首发时间:2026-10-28
  • 出版时间:2026-02-10
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  • 收稿日期:2025-03-02
  • 修回日期:2025-11-09
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    1成都医学院护理学院,四川 610036

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熊真真,E-mail:
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2种不同金属材料的力学参数
科
Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)
属
Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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