甘精胰岛素联合那格列奈与胰岛素泵对2型糖尿病骨折患者围手术期的疗效观察

分析甘精胰岛素联合那格列奈和胰岛素泵治疗2型糖尿病骨折患者围手术期的资料,发现两种治疗均能使血糖达标[空腹血糖(6.89±1.96)对(6.75±2.33)mmol/L],达标时间无显著差异[(3.6±1.6)对(2.9±1.2)d,均P0.05],但胰岛素泵组的平均血糖值更低.     

胰岛素不同的给药方式对儿童Ⅰ型糖尿病的血糖控制情况的疗效

目的探究对儿童Ⅰ型糖尿病患儿实施胰岛素不同给药方式治疗的效果及对血糖控制的影响,为临床提供指导。方法随机将2015年6月—2017年10月该院86例儿童Ⅰ型糖尿病患儿分为甲组(43例,采取胰岛素泵持续皮下注射胰岛素治疗)、乙组(43例,采取每日分多次皮下注射胰岛素治疗)。对比两组患儿的空腹血糖、餐后2 h血糖、血糖达标时间、胰岛素使用量。结果甲组患者治疗后空腹血糖[(5.65±0.39)mmol/L]、餐后2 h血糖[(7.98±2.03)mmol/L]较乙组[(6.52±0.62)mmol/L、(11.69±2.56)mmol/L]更低,差异有统计学意义(P0.05);甲组患儿血糖达标时间[(5.24±1.68)d]、胰岛素使用量[(26.24±4.30)U]、住院时间[(11.24±5.61)d]较对照组[(10.65±1.45)d、(36.94±6.61)U、(19.36±7.42)d]明显更少,差异有统计学意义(P0.05)。结论相比于每日分多次皮下注射胰岛素治疗,对儿童Ⅰ型糖尿病患儿实施胰岛素泵持续皮下注射胰岛素治疗的血糖控制效果更佳,更有助于缩短血糖达标时间。     

胰岛素泵两种基础率设定法治疗2型糖尿病比较的观察

目的 比较1段和6段法设定胰岛素泵基础率对T2DM患者疗效的影响. 方法 观察我院149例应用胰岛素泵治疗的T2DM患者,据治疗方案分为1段基础率组(A组,n=74)和6段基础率组(B组,n=75),比较两组血糖达标时间、胰岛素用量、血糖控制情况及低血糖发生率. 结果 两组达标时间差异无统计学意义;B组每日胰岛素总量[(38.2±9.26)vs(41.9±9.67) U/d,P＜0.05]及餐前量[(20.7±6.56)vs(23.15±6.12)U/d,P＜0.05]低于A组,两组基础量差异无统计学意义;达标时,两组5个时点血糖水平差异均无统计学意义,但B组一日内血糖水平标准差[(2.23±0.83)vs(2.72±1.09),P＜0.05]低于A组;B组低血糖发生率也低于A组. 结论 6段法设定胰岛素泵基础率可减少每日胰岛素用量,特别是餐前量,降低血糖波动,减少低血糖发生,更平稳地改善T2DM患者的血糖控制.     

胰岛素泵治疗2型糖尿病的临床探讨

目的比较胰岛素泵输注速效胰岛素(该研究使用诺和灵R)与多次皮下注射胰岛素治疗2型糖尿病的疗效对比。方法将2011年2月—2012年2月该院收治的68例血糖控制不佳的2型糖尿病患者自愿分为胰岛素泵强化治疗组(CSII组)和多次皮下注射岛素(MDII组)各34例,比较组间治疗过程中低血糖发生率、血糖达标时间、血糖达标时胰岛素用量。结果 CSII组与对照组MDII组比较,CSII组血糖达标时间更短[(6.4±1.8)d vs(10.6±2.5)d,P0.05],胰岛素用量更小[(0.72±0.13)U/(kg·d)vs(0.94±0.25)U/(kg·d),P0.05],治疗过程中低血糖发生(次/例)更少[(0.24±0.15)vs(0.88±0.38),P0.05],两组数据差异有统计学意义。结论 CISS疗效明显优于MDII组,安全性好,血糖达标时间更短,治疗过程中低血糖发生率更小。     

门冬胰岛素和人胰岛素强化治疗内科危重症高血糖疗效比较

目的 比较门冬胰岛素和人胰岛素强化治疗内科危重症高血糖的有效性和安全性.方法 选取中南大学湘雅二医院老年病科符合全身炎症反应综合征诊断标准的内科危重患者186例,入组时空腹血糖水平为(10.8±2.3)mmoL/L,根据患者入组时恢复进食情况分为多次皮下注射胰岛素组(MDI,n=90)和持续皮下注射胰岛素组(CSⅡ,n=96),2组均随机分为门冬胰岛素和人胰岛素亚组.MDI组中门冬胰岛素和人胰岛素亚组分别为44、46例,CSⅡ组分别为46、50例.MDI组餐前大剂量采用门冬胰岛素或人胰岛素,基础量均采用甘精胰岛素,CSⅡ组餐前大剂量及基础量均采用门冬胰岛素或人胰岛素.根据多点指尖血糖监测结果调整胰岛素用量,强化胰岛素治疗疗程7 d,使血糖控制在4.4～8.3 mmol/L,7 d后改为常规胰岛素治疗,使血糖控制在4.4～11.1 mmol/L,观察各哑组患者基线及第7天日内平均血糖水平、日内血糖标准差、日内血糖极差(最高和最低血糖之差)、血清C反应蛋白(CRP)水平、急性生理与慢性疾病评分(APACHE Ⅱ),统计7 d内低血糖发生率、严重低血糖发生率、日平均胰岛素用量及28 d内各组死亡率.统计学分析采用t检验和x~2检验.结果 (1)MDI及CSⅡ组的门冬胰岛素亚组和人胰岛素亚组强化治疗各项指标差异无统计学意义.(2)强化治疗后第7天门冬胰岛素哑组较人胰岛素组日内平均血糖水平更低,MDI组:(6.2±1.3)mmol/L比(7.6±1.6)mmol/L;CSⅡ组:(6.0±1.2)mmol/L比(7.4±2.5)mmol/L,均P＜0.05.(3)门冬胰岛素亚组血糖标准差更小,MDI组:(1.54±0.27)mmol/L比(1.92±0.38)mmol/L;CSⅡ组:(1.24±0.27)mmol/L比(1.83±0.45)mmol/L,均P＜0.05.(4)门冬胰岛素亚组极差更小,MDI组:(3.0±0.5)mmoL/L vs(3.9±1.1)mmoL/L;CSⅡ组:(3.1±0.6)mmol/L vs(3.9±1.0)mmol/L,均P＜0.05.(5)门冬胰岛素业组7 d内日平均胰岛素用量更少,低血糖发生率及严重低血糖发生率更低.同时,门冬胰岛素亚组7 d内血清CRP?     

胰岛素持续皮下注射治疗糖尿病合并脑卒中38例疗效观察

目的比较不同胰岛素给药方法治疗糖尿病合并脑卒中的疗效。方法将76例糖尿病患者分为胰岛素泵持续皮下注射(CSII)组及胰岛素多次皮下注射(MSII,4次/d)组。静脉输注5%葡萄糖溶液者,CSII组每4g葡萄糖同步增加基础量胰岛素1U;MSII组用微量注射器同步静脉注射胰岛素1U。结果治疗期间血糖平均值、血糖达标时间、低血糖(血糖2.78mmol/L)发生率两组间比较,差异均有统计学意义[(7.86±1.15)vs(10.05±1.87)mmol/L;(3.53±1.16)vs(6.49±2.75)d;23.7%vs 57.9%,P0.01];治疗后14d,两组间神经功能缺损程度(NIHSS)比较,差异有统计学意义[(21.63±4.73)vs(24.06±5.15)分,P0.05];两组间并发症发生率、死亡率比较,差异无统计学意义(23.7%vs 39.5%,5.3%vs 10.5%,P0.05)。发病后3个月,两组Barthel指数评分比较,差异有统计学意义(P0.05)。结论 CSII治疗糖尿病合并脑卒中,在血糖控制和神经功能恢复方面疗效优于MSII。     

胰岛素泵在老年2型糖尿病合并肺部感染患者中的疗效观察

目的观察应用胰岛素泵在老年2型糖尿病合并肺部感染患者中的临床疗效。方法纳入2013年11月~2015年6月在北京军区总医院住院的老年2型糖尿病合并肺部感染患者60例,其中男性42例,女性18例,年龄61~85岁,平均年龄(69.4±6.8)岁。将患者随机分为对照组和治疗组,每组各30例。对照组给予分次皮下注射胰岛素,治疗组应用胰岛素泵持续输注胰岛素。比较治疗前后两组患者的血糖水平,记录胰岛素用量及低血糖发生率。结果两组治疗第3 d和第15 d各时段血糖水平与治疗前相比均有明显下降,差异有统计学意义(P均0.01)。治疗第3 d时,治疗组的各时段血糖水平较对照组改善更明显,分别为空腹血糖[(6.3±1.2)mmol/L vs.(8.6±2.0)mmol/L],早餐后2 h血糖[(8.0±2.0)mmol/L vs.(9.5±2.2)mmol/L],晚餐前0.5 h血糖[(6.2±1.6)mmol/L vs.(8.3±2.1)mmol/L],睡前血糖[(6.9±1.4)mmol/L vs.(9.0±2.0)mmol/L],差异有统计学意义(P均0.05)。而治疗第15 d时两组各时段的血糖水平差异无统计学意义(P均0.05)。与对照组比较,治疗组的胰岛素用量少,低血糖发生率低,差异有统计学意义(P均0.05)。结论胰岛素泵对老年2型糖尿病合并肺部感染患者的血糖能起到较好的控制作用,且胰岛素用量少,低血糖发生率低。     

加用甘精胰岛素或中效胰岛素的2型糖尿病患者血糖波动的比较

目的 比较空腹血糖控制不佳的2型糖尿病患者加用甘精胰岛素(glargine)或中效胰岛素治疗对血糖波动的影响.方法 30例口服抗糖尿病药治疗的2型糖尿病患者(空腹血糖>9.0 mmoL/L,HbA1C> 8.5%),按1:1随机分成两组,分别加用甘精胰岛素(来得时(R))或中效胰岛素(诺和灵(R)N)联合治疗.以空腹指尖毛细血管血糖<6.0 mmol/L为目标,用动态血糖检测仪监测患者血糖水平,计算全天血糖水平的标准差(SDBG)、最大血糖波动幅度(LAGE)以及空腹血糖变异系数(CV-FPG)作为反映lffL糖波动的指数.结果 加用甘精胰岛素组上述三个指标均低于加用中效胰岛素组(SDBG:1.49±0.35 vs 1.73±0.46;LAGE:3.23±0.76 vs 3.73±1.00;CV-FPG 17.26±2.24 vs 3520.33±3.21,均P<0.05),同时甘精胰岛素组低血糖发生人次数也低于中效胰岛素组,但差异无统计学意义(P>0.05).结论 空腹血糖控制不佳的2型糖尿病患者加用甘精胰岛素比加用中效胰岛素治疗更有利于血糖的平稳,且不增加低血糖的风险.     

沙格列汀或格列美脲联合甘精胰岛素对2型糖尿病患者血糖波动影响的观察

目的观察沙格列汀联合甘精胰岛素及格列美脲联合甘精胰岛素对T2DM患者血糖波动的影响。方法 60例未接受胰岛素治疗且血糖控制不佳的T2DM患者被随机分为沙格列汀联合甘精胰岛素组和格列美脲联合甘精胰岛素组,共治疗12周。采用动态血糖监测系统(CGMS)监测血糖波动情况,观察BMI、FPG、HbA1c及胰岛素用量等指标。结果两组血糖控制均改善,沙格列汀联合甘精胰岛素组日内血糖平均波动幅度(MAGE)、日内血糖波动次数(NGE)、日间血糖平均绝对差(MODD)低于格列美脲联合甘精胰岛素组[(2.2±1.0)vs(4.1±1.9)mmol/L;(1.4±1.4)vs(2.6±1.5)次/d;(1.30±0.65)vs(2.60±0.90)mmol/L,P<0.05]。两组治疗后FPG及HbA1c均降低[沙格列汀联合甘精胰岛素组(10.5±2.1)vs(6.2±1.3)mmol/L,(8.7±1.2)%vs(6.3±1.1)%;格列美脲联合甘精胰岛素组(10.4±1.8)vs(6.1±1.4)mmol/L,(8.9±1.4)%vs(6.5±1.2)%](P均<0.01);沙格列汀联合甘精胰岛素组BMI低于格列美脲联合甘精胰岛素组[(22.2±2.4)vs(25.5±2.7)kg/m2](P<0.05)。结论沙格列汀联合甘精胰岛素可有效控制血糖,改善血糖波动,在血糖控制稳定性方面优于格列美脲联合甘精胰岛素。     

过氧化物体增殖物激活受体γ活化对胰岛素抵抗合并高血压大鼠代谢及血压的影响

目的探讨过氧化物体增殖物激活受体(PPAR)γ活化对高脂饮食诱发的胰岛素抵抗合并高血压大鼠代谢及血压的影响。方法30只雄性SD大鼠被随机分为正常对照组(n=10)、胰岛素抵抗合并高血压模型组(n=10)及吡格列酮治疗组(n=10)。采用高脂饮食喂饲建立胰岛素抵抗合并高血压大鼠模型,其中治疗组在喂饲高脂饮食9周后给予吡格列酮灌胃(10mg/kg.d),各组均在14周末测定大鼠血压,后处死各组大鼠,测定血糖、胰岛素、肿瘤坏死因子α(TNFα)及血清游离脂肪酸(FFA)水平。结果模型组大鼠血清胰岛素、血糖水平及血压水平均明显高于正常对照组。治疗组血清FFA[(367.3±38.1vs587.3±35.8)μmol/L,P<0.05],TNFα[(10.6±4.2vs24.3±8.8)pg/L,P<0.01],血糖[(8.2±1.3vs9.9±1.8)mmol/L,P<0.05],血清胰岛素[(30.2±5.2vs46.1±17.0)mU/L,P<0.05],血压[(142.7±15.3vs165.4±15.1)mmHg,P<0.05]均显著低于模型组,而胰岛素敏感指数显著高于模型组(4.29±1.04vs2.48±0.80,P<0.01)。结论高脂饮食等环境变化诱发的胰岛素抵抗可能在高血压的发病机制中具有重要的作用;通过促进PPARγ的活化可明显改善胰岛素抵抗,并对高血压具有一定的改善作用。     

Precipitin reactions between insulin,proinsulin, insulin chains and insulin antibody

Summary Insulin antibody was produced in guinea pigs and the precipitins tested by double diffusion in agarose gel. Pork, beef and monocomponent insulin produced precipitin lines. Proinsulin also produced a precipitin line with these antisera but no lines appeared with either the A-chain or the B-chain of insulin. There was good correlation between the precipitin titre and the radioimmunoassay titre.     

ATP sensitizes the insulin receptor to insulin

Insulin receptor with high insulin binding and tyrosine kinase activities has been prepared from human placenta. Based on a molecular mass of 306 kDa for the receptor (the value obtained from the sum of the amino acid residues), this preparation is capable of binding 1.48 mol of insulin per mol of receptor. The receptor is free from phosphatase and ATPase activity and is not stimulated by sodium vanadate. Autophosphorylation is linear with respect to receptor concentration, and the 32P incorporated is stable even in the presence of a 100-fold excess of unlabeled ATP. The Km for ATP is 208 microM. N-Ethylmaleimide inhibits autophosphorylation. Alkylation with 3H-labeled N-ethylmaleimide results in the incorporation of 1.13 +/- 0.37 mol of N-ethylmaleimide per mol of insulin binding activity exclusively into the beta subunit of the receptor. The nonhydrolyzable ATP analog adenosine 5'-[beta,gamma-imido]triphosphate stimulates autophosphorylation of the receptor, an effect that is evident at ATP concentrations below 1 mM. The stimulatory effect of adenosine 5'-[beta,gamma-imido]triphosphate is the result of increasing the binding of insulin to the alpha subunit, and this reflects itself in a shift to the left of the insulin dose-response curve for autophosphorylation. The same is true for ATP. As a consequence, it is now possible to reconcile the concentration of insulin necessary for stimulating the autophosphorylation reaction with physiological levels and with the levels of insulin required for its classical biological effects.     

Clinical utility of insulin and insulin analogs

Diabetes is a pandemic disease characterized by autoimmune, genetic and metabolic abnormalities. While insulin deficiency manifested as hyperglycemia is a common sequel of both Type-1 and Type-2 diabetes (T1DM and T2DM), it does not result from a single genetic defect—rather insulin deficiency results from the functional loss of pancreatic β cells due to multifactorial mechanisms. Since pancreatic β cells of patients with T1DM are destroyed by autoimmune reaction, these patients require daily insulin injections. Insulin resistance followed by β cell dysfunction and β cell loss is the characteristics of T2DM. Therefore, most patients with T2DM will require insulin treatment due to eventual loss of insulin secretion. Despite the evidence of early insulin treatment lowering macrovascular (coronary artery disease, peripheral arterial disease and stroke) and microvascular (diabetic nephropathy, neuropathy and retinopathy) complications of T2DM, controversy exists among physicians on how to initiate and intensify insulin therapy. The slow acting nature of regular human insulin makes its use ineffective in counteracting postprandial hyperglycemia. Instead, recombinant insulin analogs have been generated with a variable degree of specificity and action. Due to the metabolic variability among individuals, optimum blood glucose management is a formidable task to accomplish despite the presence of novel insulin analogs. In this article, we present a recent update on insulin analog structure and function with an overview of the evidence on the various insulin regimens clinically used to treat diabetes.     

Measurement of insulin absorption and insulin action

For the practical implementation of every type of insulin therapy it is necessary to know both the time course of action of therapeutically used short- and long-acting insulin preparations and the factors influencing such time-action profiles. The only reliable way to obtain the required quantitative information about the pharmacokinetic and glucodynamic properties of insulin preparations has been the use of the euglycemic glucose clamp technique. The first studies with each new insulin formulation or insulin application technique should be performed with healthy subjects in order to have the most comparable study conditions. Thereafter, results from such clinical-experimental studies should be verified in similar studies with patients with diabetes. Earlier investigational approaches, which either had been limited to the determination of the pharmacokinetic properties of insulin preparations or had used the quantitative decrease of the blood glucose level as a measure of the pharmacodynamic properties, do not provide valid quantitative results. The proposed glucose clamp technique makes possible the quantitative study of the pharmacokinetic and pharmacodynamic properties of insulin preparations under comparative and reproducible conditions.