甘精胰岛素与阿卡波糖联合治疗老年2型糖尿病的疗效观察

[目的]观察甘精胰岛素与阿卡波糖合用治疗老年2型糖尿病的疗效.[方法]对47例应用口服降糖药物血糖控制不理想的老年2型糖尿病患者应用甘精胰岛素联合阿卡波糖治疗3个月,观察治疗前后血糖、糖化血红蛋白、体重指数的变化情况以及低血糖的发生率.[结果]47例患者中有41例完成试验(其中4例因血糖控制不理想改为强化胰岛素治疗方案,2例中途退出).患者的空腹血糖、餐后2h血糖、糖化血红蛋白均较治疗前明显下降(P＜0.05),体重指数无明显变化(P＞0.05),无严重低血糖事件发生.[结论]甘精胰岛素与阿卡波糖合用对于口服降糖药物失效的老年2型糖尿病患者是一种安全、有效且方便的治疗方案.     

胰岛素泵联合口服降糖药治疗2型糖尿病的疗效比较

[目的]比较胰岛素泵分别联合吡格列酮、二甲双胍、阿卡波糖、格列美脲治疗2 型糖尿病的疗效.[方法]80例血糖控制欠佳的2型糖尿病患者停用原来治疗方案,改用胰岛素泵治疗,1周后随机分为A组、B组、C组、D组4组.A组胰岛素泵联合格列美脲,B组胰岛素泵联合吡格列酮, C组胰岛素泵联合二甲双胍, D组胰岛素泵联合阿卡波糖,共治疗4周.对比分析4组空腹血糖（FPG）、早餐后2 h血糖 （2hPG）、糖化血红蛋白（HbA1c）、胰岛素用量、血糖达标时间及低血糖发生情况.[结果]治疗后4组 FBG、2hPG 、HbA1c均较治疗前明显下降（ P 〈0.01）;四组之间胰岛素用量、血糖达标时间比较差异无显著性（ P 〈0.01）; B 、C、D组低血糖发生率差异无显著性,但均与A组比较差异有显著性（ P 〈0.01）.[结论]胰岛素泵分别联合格列美脲、吡格列酮、二甲双胍、阿卡波糖治疗能较好地控制2 型糖尿病患者血糖,但分别联合二甲双胍、阿卡波糖、吡格列酮时安全性更高.     

甘精胰岛素联合阿卡波糖对老年2型糖尿病患者血糖及β细胞功能的影响

目的观察甘精胰岛素（IG）联合阿卡波糖治疗老年2型糖尿病（T2DM）的降糖效果及对13细胞功能的影响。方法将90例口服药联合治疗空腹血糖（FPG）控制不佳的老年rr2DM患者,随机分为甘精胰岛素（IG）联合阿卡波糖组和中性鱼精蛋白锌胰岛素（NPH）组。治疗12周后比较两组治疗前后FPG、餐后2h血糖（2hPG）、糖化血红蛋白（HbAlC）、空腹C肽及餐后2hC肽水平。并对两组低血糖发生率进行比较。结果治疗12周后两组FPG、2hPG、HbAlc均下降,IG联合阿卡波糖组低血糖发生较NPH组少,治疗后c肽升高显著,与NPH组比较差异有统计学意义（P〈0．05）。结论甘精胰岛素联合阿卡波糖能较好地控制老年2型糖尿病患者血糖及糖化血红蛋白,且低血糖发生率较低,与NPH比较,安全性更高。     

甘精胰岛素联合门冬胰岛素对血糖控制不佳的2型糖尿病患者临床疗效分析

目的探讨甘精胰岛素联合门冬胰岛素治疗血糖控制不佳的2型糖尿病(T2DM)患者的临床疗效。方法将86例T2DM患者随机分为2组,每组43例。观察组给予甘精胰岛素联合门冬胰岛素,对照组给予精蛋白生物合成人胰岛素联合生物合成人胰岛素。比较治疗3个月后2组空腹血糖(FPG)、餐后2 h血糖(2 hPG)、糖化血红蛋白(HbAlc)水平的变化,以及血糖达标时间、体质量增加量、胰岛素日用量、血糖日波动量及低血糖发生率的差异。结果观察组FPG、2hPG、HbAlc水平的改善幅度大于对照组;观察组血糖达标时间、体质量增加量、血糖日波动量及低血糖发生率均显著小于对照组。结论对于血糖控制不佳的T2DM患者,甘精胰岛素与门冬胰岛素联合应用可理想控制血糖,减少体质量增加量,降低低血糖发生率,是安全而有效的胰岛素强化治疗方案。     

甘精胰岛素联合阿卡波糖治疗口服降糖药失效的2型糖尿病

目的探讨甘精胰岛素联合阿卡波糖治疗2型糖尿病患者的可行性。方法回顾性分析我院2006年9月至2009年6月64例口服降糖药失效的2型糖尿病患者应用甘精胰岛素与阿卡波糖联合治疗方案的临床资料。结果 64例患者中60例最终改为甘精胰岛素加阿卡波糖联合治疗方案获得满意血糖控制,另4例应用该方案后血糖控制仍不佳,最终改用强化治疗方案。60例患者在用甘精胰岛素加阿卡波糖方案期间从未出现低血糖。结论甘精胰岛素与阿卡波糖联合治疗的方案对于口服疗效不佳的2型糖尿病患者是一种安全、有效且方便的治疗方案,血糖控制良好,低血糖发生的可能性极小,体重明显降低。     

甘精胰岛素联合阿卡波糖治疗2型糖尿病60例分析

目的观察甘精胰岛素联合阿卡波糖治疗老年2型糖尿病的有效性及安全性。方法选择60例应用口服降糖药血糖控制不佳的老年2型糖尿病患者,停用原有口服降糖药,给予甘精胰岛素联合阿卡波糖治疗,比较治疗前后空腹血糖、餐后血糖、糖化血红蛋白、低血糖发生情况。结果 60例患者治疗12周后,空腹血糖、餐后血糖、糖化血红蛋白下降与治疗前比较差异有统计学意义,低血糖发生率低。结论老年糖尿病患者口服降糖药治疗不能使血糖控制达标的可采用甘精胰岛素联合阿卡波糖治疗,能有效的控制空腹血糖及餐后血糖,且低血糖发生率低,是安全有效的治疗方法,值得推广的治疗方案。     

甘精胰岛素与预混胰岛素分别联合口服降糖药治疗2型糖尿病患者的效果比较

目的比较甘精胰岛素与预混胰岛素分别联合口服降糖药治疗2型糖尿病(T2DM)的效果。方法 84例T2DM患者随机分为A组与B组各42例。A组给予甘精胰岛素皮下注射联合口服降糖药阿卡波糖治疗,B组给予预混胰岛素联合阿卡波糖治疗。比较2组治疗前后血糖监测值、胰岛素用量和血糖达标情况。结果 2组治疗后空腹血糖(FBG)、餐后2 h血糖(PBG)、糖化血红蛋白(Hb A1c)水平均较本组治疗前显著下降(P 0. 05)。2组治疗后FBG、PBG、Hb A1c控制达标率比较,差异均无统计学意义(P 0. 05)。A组胰岛素用量少于B组,低血糖发生率低于B组,差异均有统计学意义(P 0. 05)。2组心脑血管事件发生率比较,差异无统计学意义(P 0. 05)。结论甘精胰岛素与预混胰岛素分别联合阿卡波糖均能有效控制血糖,但甘精胰岛素联合阿卡波糖方案能显著减少胰岛素用量,降低低血糖发生率。     

甘精胰岛素联合阿卡波糖治疗老年糖尿病34例分析

目的采用甘精胰岛素联合阿卡波糖治疗老年糖尿病以评价其临床疗效。方法对34例单独使用口服降糖药血糖控制不佳的老年糖尿病患者,停用原口服降糖药,予甘精胰岛素联合阿卡波糖治疗,比较治疗前后空腹血糖(FBG)、餐后2 h血糖(PG2h)、糖化血红蛋白(HbA1c)的变化。结果治疗后FBG、PG2h、HbA1c较治疗前明显降低,且低血糖发生少。结论使用阿卡波糖联合甘精胰岛素治疗老年糖尿病安全、有效、方便。     

预混胰岛素类似物联合中午1次那格列奈治疗老年2糖尿病的效果评价

目的探讨每日两次预混胰岛素类似物注射联合二甲双胍治疗的老年2型糖尿病(T2DM)患者,空腹血糖、早餐后2小时血糖持续达标,然而糖化血红蛋白(HbA1c)却不能达标。那格列奈、阿卡波糖进一步降低HbA1c的效果及其安全性。方法采用诺和锐30早餐前和晚餐前注射联合二甲双胍治疗的T2DM老年患者43例,分为两组:A-N组(n=21)开始那格列奈120mg每日1次于午餐前服用,3个月后改为阿卡波糖50mg每日1次于午餐前服用;N-A组(n=22)开始阿卡波糖50mg每日1次于午餐前服用,3个月后改为那格列奈120mg每日1次于午餐前服用。结果治疗结束与基线比较,A-N组和N-A组HbA1c均明显降低,但两组比较差异无统计学意义。与那格列奈相比阿卡波糖的不良反应以胃肠道为主(P<0.01),那格列奈以低血糖为主但与阿卡波糖相比两者差异无统计学意义。结论每日两次注射预混胰岛素类似物联合二甲双胍是T2DM老年患者很常用的降糖方案,但是存在一些缺陷,加用那格列奈或阿卡波糖可以进一步控制血糖,与阿卡波糖相比那格列奈的胃肠道不良反应更少。     

甘精胰岛素联合阿卡波糖治疗老年2型糖尿病合并脑梗死

【目的】观察甘精胰岛素联合阿卡波糖治疗老年2型糖尿病（T2DM）合并脑梗死的疗效。【方法】80例老年T2DM合并脑梗死患者随机分为观察组和对照组各40例,观察组给予阿卡波糖50mg嚼服,每日3次;同时每天睡前皮下注射甘精胰岛素;对照组给予预混胰岛素优泌林70／30每日早晚餐前30min皮下注射;根据血糖值调整胰岛素用量。观察两组血糖控制、低血糖发生情况。采用神经功能缺损（CNN）评分判定疗效。【结果】治疗后两组空腹血糖（FPG）、餐后2h血糖（2hPG）及糖化血红蛋白（HbA1c）明显下降（P〈0．05）,观察组低血糖发生率明显低于对照组（P〈0．05）;两组治疗后CNN评分均明显改善（P〈0．05）,观察组明显优于对照组（P〈0．05）。【结论】甘精胰岛素联合阿卡渡糖治疗老年T2DM合并脑梗死疗效显著。     

地特胰岛素联合餐前速效胰岛素与胰岛素泵对2型糖尿病的疗效比较

【目的】比较地特胰岛素联合餐前速效胰岛素及胰岛素泵对2型糖尿病患者（T2DM）疗效。【方法】选取78名T2DM患者,随机分为地特胰岛素联合餐前速效胰岛素组（Ⅰ组）及胰岛素泵组（Ⅱ组）,比较两组疗效、安全性、治疗费用及生活质量等指标。【结果】两组患者治疗后血糖水平均较治疗前有显著改善（P〈0．05）,达到预期指标。Ⅱ组患者生活质量较治疗前及Ⅰ组显著提高（P〈0．05）;两组患者均未发生低血糖事件及过敏反应,Ⅱ组血糖达标时间及胰岛素用量较Ⅰ组显著降低（P〈0．05）,但费用增加（P〈0．05）。【结论】两种治疗方式各具特色,临床上应该根据患者自身情况,灵活实际地选择用药方式,以达到最佳的治疗效果。     

Poisoning with Insulin Glargine

A foodborne disease outbreak characterized by vomiting, abdominal pain and diarrhea, involving mostly children was investigated. Epidemiological, hospital and laboratory investigations indicated that the disease outbreak was associated with consumption of rancid biscuits abandoned in the street corner in a crowded locality of old city Hyderabad. The offensive flavors of rancidity were masked by the strong pineapple flavor used in the biscuits. Rancidity of the biscuits was confirmed by high peroxide value and acidity of extracted fat. Bacterial contamination was excluded by the total aerobic plate counts and negative tests for Staphylococcus and Salmonella.     

Insulin delivery with plasmid DNA

Success in controlling hyperglycemia in type I diabetics will require a restoration of basal insulin. To this end, three plasmid DNAs (pDNA) encoding preproinsulin were compared for constitutive expression and processing to insulin in nonendocrine cells in vitro. The pDNAs were designed to express rat proinsulin I (VR-3501), rat proinsulin I with the B10 aspartic acid point mutation (VR-3502), and a derivative of VR-3502 with a furin cleavage site added at the B-chain and C-peptide junction (VR-3503). Cells transfected with VR-3501 or VR-3502 were able to secrete only proinsulin, whereas transfection with VR-3503 yielded 30-70% mature insulin, which could be increased to >99% by cotransfection with a furin expression plasmid (VR-3505). The insulin produced was biologically active. The bilateral injection of 100 microg of VR-3502 plasmid into the tibialis anterior muscles of mice on two consecutive days yielded, on average, several hundred picograms of heterologous proinsulin per milliliter of serum. In BALB/c mice, serum proinsulin peaked 7-14 days postinjection and declined to preinjection levels by days 21-28. In athymic nude mice, serum proinsulin was sustained for at least 6 weeks. The therapeutic efficacy of delivering insulin via muscle injection of pDNA was evaluated in athymic nude mice made diabetic with the beta cell toxin streptozotocin (STZ). All animals given control DNA died within 1 week of receiving STZ while 40% of the mice coinjected with plasmids VR-3503 and VR-3505 lived through the duration of the 4-week experiment. Muscles of the surviving animals contained 17-100 ng of immune-reactive insulin (IRI), 86-94% of which was mature insulin. The results suggest that heterologous insulin made in muscle increased the survival rate. We propose that insulin plasmid expression in skeletal muscle may be a valid approach to basal insulin delivery. The feasibility of plasmid DNA-based delivery of basal insulin was investigated. An expression system consisting of pDNAs encoding a selectively mutated rat preproinsulin and mouse furin was developed and characterized in vitro and in vivo. When injected with preproinsulin pDNA, the mouse tibialis anterior muscle expressed and released proinsulin into serum at levels comparable to normal basal insulin in rodents. These heterologous proinsulin levels were sustained for several weeks in immune-compromised nondiabetic mice. Mouse muscle coinjected with a pDNA encoding the endopeptidase furin and a pDNA encoding a pre-proinsulin modified to contain two furin cleavage sites produced fully processed insulin. This muscle-made insulin appears to have contributed to the survival of mice treated with a highly diabetogenic dose of streptozotocin, a beta cell toxin. The results demonstrate that skeletal muscle is able to express and deliver therapeutic insulin from plasmid DNA.     

胰岛素及胰岛素抵抗与糖尿病认知功能障碍

糖尿病导致的学习记忆功能障碍日益受到人们的重视。糖尿病明显增加痴呆的发生风险,包括血管性痴呆和阿尔茨海默病;糖尿病本身也可以导致患者轻、中度认知功能的下降。胰岛素水平不足和胰岛素抵抗可明显导致糖尿病认知功能障碍的发生并加速了认知功能下降的进展。     

胰岛素泵治疗糖尿病的临床观察及护理

目的 分析胰岛素泵安置前后的护理特点并观察其疗效。方法对18例糖尿病胰岛索泵治疗的患者进行了心理、技术等全方位的综合护理。结果18例患者用胰岛素泵后血糖控制良好,胰岛素用量和低血糖发生次数减少。生活质量相应提高。结论综合护理保证了胰岛素泵控制血糖的良好效果。     

Multinational Consensus: Insulin Initiation with Insulin Degludec/Aspart (IDegAsp)

Insulin degludec/aspart (IDegAsp) is the first soluble insulin co-formulation, combining a long-acting insulin degludec (IDeg) and rapid-acting insulin aspart (IAsp). In type 2 diabetes patients with oral antidiabetes agent (OAD) inadequacy, insulin initiation with IDegAsp once daily provides superior long-term glycemic control compared to insulin glargine, with similar fasting plasma glucose (FPG) and insulin doses, and numerically lower rates of overall and nocturnal hypoglycemia. Furthermore, in patients with uncontrolled type 2 diabetes previously treated with insulins, IDegAsp twice daily effectively improves glycated hemoglobin and FPG, with fewer hypoglycemic episodes versus premix insulins and basal bolus therapy. In patients with type 1 diabetes mellitus, IDegAsp once daily with two doses of IAsp is a convenient, yet effective, regimen as compared to the conventional 4–5 injection-based basal bolus therapy. IDegAsp is an appropriate and reasonable option for initiation of insulin therapy in both type 1 and type 2 diabetes.     

Mild Electrical Stimulation with Heat Shock Ameliorates Insulin Resistance via Enhanced Insulin Signaling

Low-intensity electrical current (or mild electrical stimulation; MES) influences signal transduction and activates phosphatidylinositol-3 kinase (PI3K)/Akt pathway. Because insulin resistance is characterized by a marked reduction in insulin-stimulated PI3K-mediated activation of Akt, we asked whether MES could increase Akt phosphorylation and ameliorate insulin resistance. In addition, it was also previously reported that heat shock protein 72 (Hsp72) alleviates hyperglycemia. Thus, we applied MES in combination with heat shock (HS) to in vitro and in vivo models of insulin resistance. Here we show that 10-min treatment with MES at 5 V (0.1 ms pulse duration) together with HS at 42°C increased the phosphorylation of insulin signaling molecules such as insulin receptor substrate (IRS) and Akt in HepG2 cells maintained in high-glucose medium. MES (12 V)+mild HS treatment of high fat-fed mice also increased the phosphorylation of insulin receptor β subunit (IRβ) and Akt in mice liver. In high fat-fed mice and db/db mice, MES+HS treatment for 10 min applied twice a week for 12–15 weeks significantly decreased fasting blood glucose and insulin levels and improved insulin sensitivity. The treated mice showed significantly lower weight of visceral and subcutaneous fat, a markedly improved fatty liver and decreased size of adipocytes. Our findings indicated that the combination of MES and HS alleviated insulin resistance and improved fat metabolism in diabetes mouse models, in part, by enhancing the insulin signaling pathway.