预防性干预治疗降低1型糖尿病发病的动物实验

目的通过给予非肥胖糖尿病小鼠烟酰胺和/或卡介苗、谷氨酸脱羧酶等干预措施,探讨各种方法及联合治疗1型糖尿病的疗效。方法①实验于2000-09/2001-06在交通大学附属第一人民医院糖尿病研究室完成。选用封闭群4周龄的清洁级雌性非肥胖糖尿病小鼠85只。随机将小鼠分为5组,卡介苗组(n=15),烟酰胺组(n=15),卡介苗+烟酰胺组(n=15),谷氨酸脱羧酶组(n=15),对照组(n=25)。②卡介苗组30日龄皮内注射卡介苗0.1m L溶液(0.05m g),31～89日龄每天腹腔注射生理盐水0.1m L,90日龄时干预措施同30日龄时。烟酰胺组30～90日龄按500m g/(kg·d)剂量腹腔注射烟酰胺,使用时稀释至0.1m L。卡介苗+烟酰胺组30日龄皮内注射卡介苗溶液0.1m L(0.05m g),31～89日龄按500m g/(kg·d)剂量腹腔注射烟酰胺,使用时稀释至0.1m L,90日龄时干预措施同30日龄时。谷氨酸脱羧酶组30日龄时按0.5m g/只,每只管饲谷氨酸脱羧酶溶液0.1m L,31～90日龄每天腹腔注射生理盐水0.1m L。对照组30～90日龄每天腹腔注射生理盐水0.1m L。自第5周起每周测体质量一次,每日测定各组的饮食及饮水量。非肥胖糖尿病小鼠自出生第90天起,每周用雅培血糖仪测一次尾静脉随机血糖,连续2次血糖≥11.1m m ol/L,诊断为糖尿病。③确诊为糖尿病后每周测1次随机血糖。采用高压液相法测定糖化血红蛋白。采用定量酶联免疫吸附法测定谷氨酸脱羧酶、IA-2抗体。采用光镜观察β细胞破坏程度及淋巴细胞浸润情况,每张胰腺切片中随机计数10个胰岛的胰岛炎评分总和。胰岛炎评分标准共分7级。0分胰岛周围无淋巴细胞浸润。1分胰岛周围局部淋巴细胞浸润。2分胰岛内有部分淋巴细胞浸润,范围<1/3。3分胰岛内有较多淋巴细胞浸润,范围1/3～1/2。4分胰岛内有大量淋巴细胞浸润,范围>1/2,但未达到100%。5分全胰岛炎(整个胰岛全部被淋巴细胞浸润)。6分胰岛萎缩。④组间变量比较用两样本均数t检验,组间比较用成组t检验。结果在实验期间共有2只非肥胖糖尿病小鼠意外死亡对照组及卡介苗+烟酰胺组各1只,进入结果分析对照组24只,卡介苗组、烟酰胺组、谷氨酸脱羧酶组各15只,卡介苗+烟酰胺组14只。①4个治疗组小鼠糖尿病发病率明显低于对照组[42%(10/24),8%(5/59),P<0.01]。烟酰胺组2只、卡介苗组2只、卡介苗+烟酰胺组1只、谷氨酸脱羧酶组0只发病,各组发病率分别为13%(2/15),13%(2/15),7%(1/14),0。②烟酰胺组、卡介苗组与对照组谷氨酸脱羧酶抗体滴度比较,差异不明显,卡介苗+烟酰胺组谷氨酸脱羧酶抗体滴度明显高于对照组(P<0.05),谷氨酸脱羧酶组谷氨酸脱羧酶抗体滴度则为0。各干预治疗组胰岛炎评分均明显低于对照组(P<0.05)。③所有非肥胖糖尿病小鼠蛋白酪氨酸磷酸酶抗体IA-2A滴度均为0。结论①在自身免疫性胰岛炎发生前给予烟酰胺、卡介苗及谷氨酸脱羧酶等干预治疗可减轻或延缓非肥胖糖尿病小鼠自身免疫性胰岛炎而减少糖尿病的发病。②非肥胖糖尿病小鼠糖尿病的发病与胰岛炎程度密切相关,当非肥胖糖尿病小鼠胰岛炎达到一定程度时,就发生了糖尿病。③谷氨酸脱羧酶抗体水平与糖尿病的发病不呈平行关系。④卡介苗和/或烟酰胺不是通过抑制抗体的生成从而降低糖尿病的发病的。⑤蛋白酪氨酸磷酸酶与非肥胖糖尿病小鼠糖尿病的发病无关。     

2型糖尿病患者真胰岛素的检测和分析

目的　采用酶联免疫法测定真胰岛素 (TI)水平 ,探讨其在 2型糖尿病 (DM)患者胰岛 β细胞功能中的意义。方法　对 99例对象 [其中DM 39例 ,糖耐量低减 (IGT) 30例 ,正常糖耐量 (NGT) 30例 ],行口服 75 g葡萄糖耐量试验及TI、胰岛素 (INS)和C肽 (CP)释放试验 ,进行比较。结果　以酶联免疫法测定的TI值 ,各组TI值均低于放射免疫法测定的INS值 ;空腹TI值NGT组 >IGT组 >DM组 ,INS值DM组 >IGT组 >NGT组。结论　TI的测定比INS的测定更敏感、更准确     

短期胰岛素泵强化治疗对初诊2型糖尿病患者胰岛β细胞功能的影响

【目的】探讨短期胰岛素泵强化治疗对初诊2型糖尿病(T2DM)患者胰岛β细胞功能的影响。【方法】对30例初诊T2DM患者进行为期两周胰岛素泵强化治疗,分析比较治疗前后空腹FPG及餐后2h血糖(2hPG)、糖化血红蛋白(HbA1C)、静脉葡萄糖耐量试验时第一时相胰岛素及C肽分泌。【结果】胰岛素强化治疗后,FPG、2hPG、HbA1C均较前明显下降(P<0.01),空腹及第一时相胰岛素和C肽的分泌较前明显升高(P<0.01)。【结论】短期胰岛素泵强化治疗可明显改善初诊2型糖尿病患者胰岛β细胞功能。     

2型糖尿病家系一级亲属非糖尿病患者绝经后胰岛功能研究

【目的】研究2型糖尿病家系一级亲属非糖尿病患者绝经后的胰岛功能。【方法】2型糖尿病家系非糖尿病一级亲属组（FDR）89例和正常对照组（NC）62例,测定人体测量指标、血糖、胰岛素、血脂等。【结果】与NC组比较,FDR组糖调节受损（IGR）增加,β细胞功能指数（MBCI）和处置指数（DI）下降。由MBCI获得的DI值与年龄、家族史等相关。【结论】糖尿病家族史影响绝经后非糖尿病的2型糖尿病一级亲属的糖代谢异常和胰岛β细胞功能。     

山药参芪丸治疗老年2型糖尿病的综合护理干预

[目的]探讨护理干预对中药组方山药参芪丸治疗老年人2型糖尿病的血糖水平的影响.[方法]将156例使用山药参芪丸治疗的老年2型糖尿病患者随机分为干预组和对照组各78例,干预组实施综合护理干预,对照组实施常规护理.治疗3个月后比较两组患者的血糖水平.[结果]两组治疗干预后空腹血糖、餐后2小时血糖及糖化血红蛋白均明显下降（P〈0.01,P〈0.05）,干预组下降更为显著（P〈均0.05）.[结论]综合护理干预措施可以提高老年2型糖尿病患者自我管理、自我保健意识和治疗的依从性,有效控制血糖水平     

老年2型糖尿病患者胰岛α细胞功能评估

目的：初步了解老年发病的2型糖尿病患者胰岛β细胞功能。以期为老年糖尿病预防及早期康复措施的介入提供理论依据。方法：2000—06／2004—06在北京大学人民医院门诊及内分泌科、老年科住院治疗的中年糖尿病患者111例(中年组)，男69例，女42例。同期在北京大学人民医院老年门诊及老年科住院治疗老年糖尿病患者72例(老年组)。男41例。女30例。测定两组患者口服葡萄糖耐量试验各点血糖、胰岛素等指标，计算各项胰岛素抵抗指数及β细胞功能指数。并将年龄与各项指标作Pearson相关分析。结果：①老年组患者口服葡萄糖耐量试验0，30，60。120min血糖值【(7．6&;#177;2．9)，(11．8&;#177;3．5)。(15．4&;#177;4．4)，(15．5&;#177;5．1)mmol／L】均低于中年组【(8．7&;#177;3．1)。(14．1&;#177;3．7)。(17．4&;#177;3．9)．(17.0&;#177;4．2)mmol／L】【t=2．225—3．270，P&;lt;0．05～0．01）；老年组患者120，180min胰岛素水平均高于中年组(t=3．114，t=2．005，P&;lt;0．05)。老年组糖负荷后30min胰岛素增值与血糖增值的比值高于中年组(t=2．42，P&;lt;0．05)。②在老年2型糖尿病组中，年龄与稳态模式评估法评估β细胞功能指数呈显著正相关(r=0．314，P&;lt;0．01)，与其余指标无显著相关性。结论：老年发病的2型糖尿病患者与中年发病者相比，具有相对较高的β细胞功能水平。     

非胰岛素依赖型糖尿病发病机制

<正>非胰岛素依赖型糖尿病(NIDDM)发病机制涉及遗传和环境因素,临床表现为异质性特征,不同亚组发病机制有所不同,现就目前公认的有关机制讨论如下.1 NIDDM胰腺病理和功能特征NIDDM患者B细胞显著减少,A细胞(分泌胰高血糖素)增加,D细胞(分泌生长抑素)减少,90%以上有胰岛淀粉样物质(主要由淀粉样多肽即IA-PP或Amylin组成)沉积,但老年非糖尿病人胰岛也可见少量Amylin,NIDDM者如无Amylin则可能是一种不同的亚组.早期NIDDM基础胰岛素(INS)分泌正常或升高,但与升高的血糖比值相对是低的.正常人静注葡萄糖后2～3分钟内INS分泌升高,为第一时相峰,迅速下降,到10分钟后又缓慢分泌增加,至少持续60分钟,称第二时相峰.NIDDM常缺乏第一时相峰,导致     

短期胰岛素泵强化治疗初诊2型糖尿病患者疗效

近年研究表明，糖尿病患者的长期、持续的高血糖，对机体是一种中毒状态。它可引起特异性的组织损伤，广泛的引起全身微血管、大血管、肌肉、脂肪、胰腺B细胞的功能和结构改变，最终导致一系列慢性并发症的发生，即“糖毒性’’作用。狭义的糖毒性作用系指对B细胞的特异性毒性作用。“糖毒性”一个重要特点是起始时的可逆性，持续性皮下胰岛     

Immune intervention for type 1 diabetes mellitus

The major form of type 1 diabetes (T1D) is characterised by immune-mediated pancreatic islet β-cell destruction, and has also been called type 1A diabetes to distinguish it from idiopathic forms of islet β-cell loss. Since the first demonstration of islet cell antibodies in 1974, the concept has been that this form of diabetes is autoimmune in nature. The commonly accepted concept is that antibodies (representing the humoral arm of the immune system) do not mediate the β-cell destruction but rather serve as markers of that destruction, while the cellular arm of the immune system, specifically T-lymphocytes, mediate the β-cell destruction. Yet, the T-lymphocytes do not act alone. They receive help in initiating the response from antigen-presenting cells such as dendritic cells and macrophages, and appear to receive help also from B-lymphocytes. In addition, the initial immune response engenders secondary and tertiary responses - involving the whole immunological army - which collectively result in impairment of β-cell function, progressive destruction of β-cells, and consequent development of type 1A diabetes. The process is insidious and may evolve over many years, with the overt expression of clinical symptoms becoming apparent only when most β-cells have been destroyed. Yet, the process clearly evolves at different speeds - much more rapidly in young children, much more slowly in older individuals. And, although it has been thought that ultimately there is complete β-cell destruction, several studies have now demonstrated some degree of persistent β-cell function or existence (at autopsy) in long-standing T1D. A major focus of investigation in T1D is the preservation of β-cell function (and, it is hoped, of β-cells themselves), in the expectation that continuing endogenous insulin secretion will contribute towards better glycaemic control, reduce episodes of severe hypoglycaemia, and slow the development of complications such as retinopathy and nephropathy. Thus, there have been many studies designed to interdict the T1D disease process, mostly by altering the immune system, both during the stage of evolution of the disease and at the time of disease onset. This chapter of the Yearbook of Advanced Technology and Treatments in Diabetes reviews the key papers that have appeared in this field between July 2009 and June 2010. Articles selected were confined to studies in human beings. All immune intervention studies reported in this time frame were included. In addition, the author selected other relevant articles dealing with mechanisms, markers, triggers, and pathology of human type 1 diabetes.     

护理干预对降低老年糖尿病患者强化治疗期间低血糖发生率的效果评价

目的 了解护理干预措施在降低老年糖尿病患者胰岛素强化治疗中低血糖发生率的应用价值,以有效降低低血糖的发生率.方法 将2009年1月至2010年1月收住我科需进行胰岛素强化治疗的450例老年糖尿病患者,随机分为干预组280例和对照组170例.回顾分析干预组和对照组不同程度低血糖症状构成比及干预前、后血糖值.结果 干预组和对照组不同程度低血糖症状构成比对照显示,意识障碍者和无症状者构成比差异显著,轻度症状者构成比无显著差异.干预组和对照组干预前、后血糖值对照显示,干预前血糖值无显著差异,干预后血糖值差异显著.所有患者无发展为低血糖昏迷或酮症酸中毒者,无死亡病例出现.结论 常规护理基础之上加用护理干预措施,能增加老年糖尿病患者使用胰岛素的知识,强化治疗期间规范应用胰岛素,显著降低低血糖症状的发生率.     

运动干预对降低妊娠期糖尿病发生的效果评价

目的探讨运动干预对降低妊娠期糖尿病(gestational diabetes mellitus,GDM)发生的效果。方法将2016年1月至2017年12月在吕梁市卫生学校附属医院妇产科行门诊常规产检的387名孕妇按产检就诊顺位编号分为观察组(194人)与对照组(193人)。对照组采取产检常规护理干预;观察组在对照组基础上加入个性化运动指导、咨询、随访与监督、精神支持等运动干预。比较两组运动自我效能及GDM发生情况。结果对照组运动自我效能3个维度得分及总得分均低于观察组(P <0. 01);观察组GDM发生率为6. 19%(12/194),明显低于对照组GDM发生率[19. 17%(37/193)](P<0. 01)。结论运动干预能有效降低妊娠期糖尿病的发生率。     

护理干预对2型糖尿病病人的影响

[目的]提高2型糖尿病病人健康知识水平和自控行为，帮助病人实现治疗的最佳目标。[方法]用随机单盲对照法将120例糖尿病病人分为A组和B组，A组进行分组强化干预，并针对每位病人进行个体指导；B组仅进行一般的糖尿病知识教育。6个月后监测病人糖尿病知识、自控行为及血糖、糖化血红蛋白变化。[结果]A组糖尿病知识了解、自控行为人数明显高于B组（P〈0．05），血糖、糖化血红蛋白值明显低于B组。[结论]实施分组强化的护理干预，比一般的教育指导更能有效提高病人自控能力，增强病人对糖尿病的认识，对控制和稳定血糖有积极意义。     

Cell therapies for type 1 diabetes mellitus

Type 1 diabetes is caused by autoimmune destruction of pancreatic beta-cells and is characterised by absolute insulin insufficiency. The monocellular nature of this disease and endocrine action of insulin make this disease an excellent candidate for cellular therapy. Furthermore, precedent for cellular therapies has been set by successful cadaveric whole pancreas and islet transplantation. In order to expand the supply of cells to meet current and future needs, several novel cell sources have been proposed, including human beta-cells or islets expanded in culture, islet xenografts and pancreatic ductal progenitor cells. Surrogate beta-cells derived from hepatocytes, intestinal K cells or non-endodermal cell types have also been suggested. Stem cells found in bone marrow and umbilical cord blood have been used extensively to repopulate the haematopoietic system and offer the possibility of autologous transplantation. Recent studies have suggested that these stem cells may also have a broader capacity to differentiate, possibly into beta-cells. Stem cells from embryonic sources, such as human embryonic stem and embryonic germ cells, have the ability to proliferate extensively in culture and have an inherent developmental plasticity that may make them a potentially unlimited source of cells that can sense glucose and produce mature insulin. The wide range of proposed cell sources and our increasingly clear picture of pancreatic development suggest that novel cellular therapies might one day compete with non-cellular glucose sensing and insulin delivery devices.     

Increased incidence of type II diabetes mellitus in Mexican Americans

OBJECTIVE: To determine whether Mexican Americans have an increased incidence of non-insulin-dependent (type II) diabetes mellitus relative to non-Hispanic whites. Currently, no study has reported on the incidence of this disorder in Mexican Americans. RESEARCH DESIGN AND METHODS: We determined the 8-yr incidence of type II diabetes in 617 Mexican Americans and 306 non-Hispanic whites who participated in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Forty Mexican Americans (6.5%) and 6 non-Hispanic whites (2%) developed type II diabetes, as defined by World Health Organization criteria. The age-adjusted ethnic odds ratio (OR; Mexican Americans/non-Hispanic whites) for diabetes incidence was 8.13 (95% confidence interval [C1] 1.10-59.9) in men and 3.62 (95% CI 1.37-9.55) in women. We adjusted for age, sex, ethnicity, body mass index, and level of educational attainment with multiple logistic regression analyses. RESULTS: Mexican Americans continued to show a statistically significant increase in diabetes incidence (OR 2.72, 95% CI 1.02-7.28). Obesity and age were also positively related to diabetes incidence in this analysis (P less than 0.001). In addition, subjects with at least some college education had a lower incidence of diabetes than those with less than a high school education (OR 0.51, 95% CI 0.26-0.99). CONCLUSIONS: The incidence of type II diabetes in Mexican Americans is greater than in non-Hispanic whites, a difference that is not explained by ethnic differences in obesity, age, or level of educational attainment.     

Modern insulin therapy for type 1 diabetes mellitus

Modern insulin therapy for Type 1 diabetes is part of a comprehensive treatment program designed to achieve and maintain blood glucose levels as close to normal as possible. The insulin regimens most likely to be successful approximate physiologic insulin delivery by combining basal and meal doses. Several options are available, including constant infusion by external pump and multiple daily injection therapy. Modern therapy affords major health benefits through improved blood glucose control, as well as lifestyle benefits associated with increased flexibility and spontaneity.