甘精胰岛素联合瑞格列奈治疗老年2型糖尿病患者的疗效与安全性

目的 观察甘精胰岛素注射液联合口服降糖药物瑞格列奈对老年2型糖尿病患者的血糖控制情况和低血糖的风险. 方法 选择口服降糖药物血糖控制不良的老年2型糖尿病患者64例,随机分为甘精胰岛素组(简称甘精组)和预混胰岛素组(诺和灵30R,简称预混组),每组各32例.甘精组在每天3餐前口服瑞格列奈的基础上,每晚22时注射甘精胰岛素1次;预混组每天早、晚餐前分别注射诺和灵30R预混胰岛素;根据空腹血糖及餐后血糖的水平,每3天调整瑞格列奈及胰岛素剂量,以空腹血糖<7.2 mmol/L,餐后血糖<10.0 mmol/L为治疗目标,共治疗16周,观察血糖控制和低血糖发生情况. 结果 治疗16周后两组的全天血糖谱和糖化血红蛋白(HbAlc)有明显下降(P<0.05),甘精组全天各时点血糖均值低于预混组,其中午餐后、晚餐后2 h血糖与预混组比较,差异有统计学意义(均为P<0.05),甘精组HbAlc值明显低于预混组(P<0.05);体质指数(BMI)甘精组无明显增加(P>0.05),预混组BMI较治疗前明显增加(P相似文献   

甘精胰岛素联合口服降糖药与预混胰岛素对2型糖尿病患者血糖控制稳定性的影响

目的 对比短期内甘精胰岛素联合口服降糖药与预混胰岛素对2型糖尿病患者血糖控制、血糖稳定性及安全性的影响.方法 连续入选60例因血糖控制不佳初次使用胰岛素的2型糖尿病住院患者,随机分为甘精胰岛素联合口服降糖药物组(甘精组)和预混胰岛素组(预混组),分别给予甘精胰岛素每日一次皮下注射联合餐前口服降糖药以及给予门冬胰岛素30注射液每日两次皮下注射治疗.开始治疗2 w后,采用动态血监测测系统(CGMS)观察血糖波动情况,同时记录患者全天指血血糖并与人院时比较,记录患者胰岛素使用量以及低血糖情况.结果 两组患者入组时一般临床特征及生化指标无显著差异;治疗2 w后CGMS监测两组平均血糖(MBG),高血糖曲线下面积(AUC)无明显差别,甘精组血糖标准差(SD)、日内平均血糖波动幅度(MAGE)、低血糖曲线下面积(AUC)均显著低于预混组;甘精组胰岛素使用量及低血糖发生率显著低于预混组(均P＜0.05).结论 与预混胰岛素比较,甘精胰岛素联合口服降糖药物治疗2型糖尿病,降糖效果相当,血糖波动更小,低血糖发生率低.     

甘精胰岛素对老年2型糖尿病患者降糖的疗效观察

选取68例老年(年龄>65岁)2型糖尿病患者,起始三天停用原来降糖药物,第四天起给予中效胰岛素(NPH)联合餐前短效胰岛素皮下注射强化胰岛素治疗,血糖相对平稳后,分为二组,分别采用睡前注射甘精胰岛素联合那格列奈口服和预混30R胰岛素皮下注射治疗12周。比较治疗后两组血糖达标时间、平均空腹血糖、血糖漂移、胰岛素用量、低血糖发生率。结果:甘精胰岛素组在血糖达标时间、治疗后空腹血糖、日内血糖漂移、低血糖发生率方面均低于预混胰岛素组(P<0.05)。结论:老年冠心病合并2型糖尿病患者中,甘精胰岛素联合那格列奈治疗,疗效确切、易于接受、低血糖反应少。     

甘精胰岛素联合瑞格列奈治疗2型糖尿病90例的可行性观察

目的分析应用甘精胰岛素联合瑞格列奈对2型糖尿病进行治疗的临床相关及价值。方法选择2013年1月—2014年3月在该院接受治疗的90例2型糖尿病患者随机平分为观察组、对照组各45例。对对照组进行预混胰岛素皮下注射治疗,对观察组进行甘精胰岛素皮下注射联合瑞格列奈口服治疗。结果观察组Hb A1C水平、胰岛素用量、低血糖发生率均显著比对照组要低(P0.05)。结论应用甘精胰岛素联合瑞格列奈对2型糖尿病进行治疗,可有效提高临床疗效,是2型糖尿病的理想治疗方式。     

甘精胰岛素与瑞格列奈联用治疗2型糖尿病的临床研究

目的 观察甘精胰岛素联合瑞格列奈治疗2型糖尿病临床疗效.方法 常规治疗糖尿病基础上,对照组早晚餐前30min注射诺和灵30R 0.3～1.0U·kg-1·d-1;观察组每餐前15min口服瑞格列奈1mg,3次/d,根据餐后2h血糖每3d调整瑞格列奈量,最大量为4mg,3次/d;每晚睡前注射甘精胰岛素,起始剂量为0.1U·kg-1·d-1,剂量均根据患者的病情进行个体化调整.治疗前后测定两组患者空腹血糖、早餐后2h血糖及糖化血红蛋白(HbA1c)水平;观察胰岛素用量、体质量和BMI、低血糖事件发生率及安全性指标.结果 观察组患者空腹血糖、早餐后2h血糖、胰岛素用量、体质量和BMI、低血糖事件发生明显改善,优于对照组,未见明显不良反应.两组总有效率比较,差异有统计学意义(P＜0.05).结论 甘精胰岛素联合瑞格列奈治疗2型糖尿病临床疗效良好,值得推广.     

甘精胰岛素联合阿卡波糖治疗非肥胖2型糖尿病临床观察

目的 评价甘精胰岛素联合阿卡波糖对非肥胖2型糖尿病血糖控制及低血糖事件的影响.方法 非肥胖2型糖尿病患者49例,分为甘精胰岛素联合阿卡波糖组(24例)应用甘精胰岛素日一次皮下注射配合阿卡波糖片日三次口服;预混人胰岛素组(25例)应用预混型人胰岛素70/30早晚餐前30分钟皮下注射.12周后随访血糖控制和低血糖事件发生情况.结果 两组空腹血糖,餐后2小时血糖,糖化血红蛋白较治疗前明显下降(P＜0.01).甘精胰岛素联合阿卡波糖组空腹血糖控制优于B组[(6.63±0.73)mmol/ L 对(7.21±0.88)mmol/ L )](P＜0.05),甘精胰岛素联合阿卡波糖组2例,预混人胰岛素组8例出现低血糖,两组比较差异有显著性(P＜0.05).结论 甘精胰岛素与阿卡波糖联合应用更好地改善了血糖控制,减少了低血糖发生率,增加了患者依从性.     

甘精胰岛素联合口服降糖药和诺和锐30治疗2型糖尿病的比较

60例口服降糖药血糖控制不良的T2DM患者随机分为甘精组,n=30和预混组,n=30,所有患者以二甲双胍作为基础用药,后血糖控制不良者酌情加用瑞格列奈;预混组每日餐前分别注射2～3次诺和锐30。根据血糖水平调整胰岛素剂量,观察12周。结果:两组治疗后血糖及HbA1c较前明显下降、C肽分泌改善(P0.01),甘精组空腹血糖下降更明显(P0.05)、空腹血糖达标时间缩短、低血糖发生率低、胰岛素用量明显减少(P0.01)并且体重无明显改变(P0.05)。结论:以二甲双胍为基础治疗措施的T2DM患者联合甘精胰岛素、瑞格列奈治疗可以有效降低血糖,空腹血糖控制更低、更快,对体重影响小,低血糖发生率低。     

甘精胰岛素治疗预混胰岛素疗效不佳糖尿病患者临床研究

将54例预混胰岛素疗效不佳的2型糖尿病患者随机分为加用甘精胰岛素组（A组）、加用中效胰岛素组（B组）及强化治疗组（C组）。治疗12周后比较糖化血红蛋白（HbA1c）水平、每天各时点指尖血糖水平、低血糖发生率及患者依从性。发现三组均可以获得较好的血糖控制,HbA1c明显下降。A组凌晨2点血糖比B组及C组更安全,A组低血糖发生率更低,患者治疗依从性更高。提示预混胰岛素疗效不佳的2型糖尿病患者睡前加用甘精胰岛素治疗,降糖效果显著,安全性高,依从性好。     

甘精胰岛素结合瑞格列奈治疗2型糖尿病50例临床效果观察

目的观察甘精胰岛素结合瑞格列奈治疗2型糖尿病的临床效果。方法选取2013年10月—2014年10月来该院进行治疗的2型糖尿病患者100例,在其知情并同意的情况下分为对照组和观察组,每组50例。对照组患者采用预混胰岛素进行治疗,观察组患者采用甘精胰岛素结合瑞格列奈进行治疗,观察两组患者治疗的情况。结果两组患者经过治疗后糖化红蛋白,2 h PG、空腹血糖水平均有所下降,但是观察组患者的治疗效果更为明显,差异有统计学意义(P<0.05)。结论 2型糖尿病患者在治疗上采用甘精胰岛素结合瑞格列奈的方式具有维持血糖稳定、减少胰岛素使用量、低血糖情况发生率低的特点,能够提升治疗的总体效果和患者的生存质量,是临床治疗中较为理想的治疗方案,值得推广应用。     

甘精胰岛素联合瑞格列奈与预混胰岛素治疗比较

56例口服降糖药血糖控制不理想的T2DM患者随机分为甘精胰岛素治疗组（n=30）和预混胰岛素组（n=26）。以两组FBG均达到〈6．1mmol／L为目标，共12周，结果：两组血糖均明显下降，甘精胰岛素组下降更显著，低血糖事件更少；结论：长效胰岛素联合瑞格列奈使继发性失效的T2DM患者血糖达标更好，低血糖事件的发生更少，依从性大大提高。     

Serum insulin,insulin antibodies and insulin requirement in the first period of insulin treatment in non-insulin resistant diabetics

Summary Twelve insulin-sensitive diabetics were studied for 200 days after the initiation of mixed beef-pork NPH insulin. Normalization of the fasting blood glucose was not accompanied by any elevation in the pre-treatment fasting immunoreactive insulin level. Insulin antibodies appeared in 2 patients on the second week of insulin treatment, in 6 others within 87 days. In 4 patients no antibodies were found 200 days after the start of insulin. The appearance of antibodies was accompanied in two patients by a decrease in insulin requirement, in others there was no change. When antibodies were present, the total maximum insulin binding capacity was 4 to 12 U/1, but the total insulin constituted only 3 to 36% of the binding capacity. Insulin wastage caused by the destruction of the immune complexes was calculated to be 0.35 to 5.6 U/die only, and this explains the negligible effect of insulin antibodies on insulin requirement in non-resistant patients. Presented at the 10th Annual Meeting of the European Association for the Study of Diabetes in Jerusalem, September 11–13, 1974.     

Characterization of circulating insulin in insulin autoimmune syndrome

We examined the forms of circulating insulin in three patients with the insulin autoimmune syndrome by a method combining gel filtration and reverse phase high performance liquid chromatography (RP-HPLC). Insulin bound to circulating antibody was dissociated by molecular sieve chromatography at acid pH. The free insulin peak eluted from a Sephadex G-50 column was subsequently chromatographed on a Bio-Gel P-30 column. In all three patients, insulin coeluted with normal human insulin. However, when the partially purified insulins, obtained by gel filtration, were applied to RP-HPLC, an abnormally migrating insulin was found in two of three patients. The insulins were more hydrophobic than normal human, porcine, or bovine insulin, but were different from each other. A third patient had only a single insulin peak on RP-HPLC which corresponded to normal insulin. In contrast, the insulin from insulin-treated diabetic patients with antibodies to exogenous insulin corresponded to either porcine or bovine and normal human insulin. The antibodies in the circulation of these patients with the autoimmune syndrome were of the immunoglobulin G type and contained kappa and lambda-chains in the same proportions as antibodies in insulin-treated patients. Autoantibodies could not be distinguished from those secondary to exogenous insulin treatment on the basis of displacement of binding by human, beef, or pork insulin. These results suggest that in certain patients with the insulin autoimmune syndrome, there may be a molecular abnormality of circulating insulin. Whether this comprises a cause for the syndrome or is a result of posttranslational processing of insulin remains to be determined.     

Relationship between insulin resistance, insulin secretion and insulin metabolism in simple obesity

The study was designed to evaluate whether the correlation occurring in simple obesity between insulin resistance and peripheral hyperinsulinemia corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. In addition, the study investigated the relation existing in simple obesity between insulin resistance and insulin metabolism. For these purposes, we measured and correlated: (1) insulin sensitivity, estimated by glucose disappearance rate from plasma after intravenous insulin injection; (2) insulin secretion by the pancreas, estimated by fasting C-peptide levels in peripheral blood; (3) insulin metabolism, estimated by means of C-peptide: insulin molar ratio in peripheral blood. Twenty-five subjects (20 females, five males) aged 21 to 59 years were studied. All were obese and had a normal glucose tolerance. Glucose disappearance rate from plasma after i.v. insulin injection averaged 3.65 +/- 0.42 mg/dl/min (mean +/- s.e.m.). Fasting C-peptide was 0.90 +/- 0.09 nmol/l. Fasting C-peptide: insulin molar ratio averaged 5.94 +/- 0.48. Negative correlations were found between glucose disappearance rates after i.v. insulin injection, ie, insulin sensitivity, and fasting concentrations of both insulin (r = -0.806, P less than 0.001) and C-peptide (r = -0.525, P less than 0.01). A positive relationship was found between glucose disappearance rate from plasma after i.v. insulin injection and fasting C-peptide: insulin molar ratio, ie, insulin metabolism (r = 0.707, P less than 0.001). We conclude that in simple obesity insulin overproduction by the pancreas is negatively related to insulin resistance, and insulin resistance and impaired insulin metabolism are strictly related phenomena.     

Overnight basal insulin requirements in insulin dependent diabetics

Programming open loop insulin delivery systems makes necessary the knowledge of patients insulin needs. It is frequently postulated that insulin needs increase at the end of the night in relation to the rise in cortisol secretion. According to this hypothesis is it justified to speed up the insulin infusion rate in the early morning? This question was addressed by studying insulin infusion rate by an artificial pancreas during the night in 12 C. peptide negative insulin dependent diabetics. They were connected to the artificial pancreas from 8 a.m. to 10 a.m. the next morning while on their habitual diabetic diet and slept as usual from 11 p.m. to 7 a.m. approximately. From 11 p.m. to 7 a.m. mean insulin infusion rate was 21.5 +/- 3.3 mU/Kg/h representing 15.6 +/- 1.6% of the dose delivered in 24 hours. Blood glucose was stable around 85 mg/dl. No significant differences were observed in the hourly insulin infusion rate during the night period, in spite of a slight tendency to a rise (from 21.1 +/- 2.8 to 22.1 +/- 2.6 mU/kg/h) tendency to a rise (from 21.1 +/- 2.8 to 22.1 +/- 2.6 mU/kg/h) after 4 a.m. On the basis of these results obtained in patients sleeping as usual it does not appear useful to envisage a systematic acceleration of insulin infusion rate by continuous delivery systems in the early morning.     

免疫原性与特异性胰岛素检测对胰岛β细胞功能评估的比较

在不同糖耐量者同时检测免疫原性胰岛素(IRI)与特异性胰岛素,发现虽然数值不同,但两种测定方法对于评估不同糖耐量者胰岛β细胞分泌功能及胰岛素敏感性的效果是一致的,提示测定IRI仍有临床实用价值.     

Role of insulin in glucose-stimulated insulin secretion in beta cells

Diabetes is on the increase worldwide and greater than 90% are type 2. There are two features to type 2 diabetes: muscle, fat and liver tissues are insulin resistant and beta cells lose the ability to secrete insulin. Prior to developing diabetes, however, insulin resistant individuals lose the first-phase insulin secretion response. Transgenic mice lacking insulin receptors in their beta cells have no first-phase response. Primary cultures of mouse islets pre-exposed to anti-insulin do not exhibit a first-phase insulin secretion response. That is, beta cells, like muscle, fat, and liver, are an insulin sensitive tissue and in the presence of insulin resistance (type 2 diabetes), in the absence of insulin receptors (transgenic mice lacking beta cell insulin receptors), or in the absence of constitutively secreted insulin (anti-insulin treatment), beta cells are unable to respond properly to post-prandial glucose. The purpose of this report is to review our understanding of the glucose-stimulus response and of insulin signaling, and to suggest why the latter may be necessary for the former to proceed.     

Influence of insulin treatment on insulin sensitivity in insulin requiring type 2 diabetes patients

Insulin resistance in type 2 diabetes subjects was investigated before and 6 months after insulin administration in 43 type 2 diabetes patients (28 females and 15 males). Their age was 56.1+/-8.6 years, diabetes duration 11.7+/-6.8 years, BMI 29.5+/-5.3 kg/m2. All patients were on maximal dosage of oral hypoglycaemic agents and had poor metabolic control (HbA1c 11.2+/-1.6%). Insulin sensitivity was measured by euglycaemic clamp (insulin infusion rate 1 mU kg-1 min-1). The glucose disposal rate (M-value) was considerably lower in patients (2.4+/-1.6 mg kg-1 min-1, 0.2-8.1) compared with healthy subjects (7.1+/-0.2 mg kg-1 min-1, p<0.01). M-value was strongly associated with WHR (r=-0.41, p<0.05). The patients with poorest insulin sensitivity had the highest level of total cholesterol (r=-0.41, p=0.02) and LDL-cholesterol (r=-0.38, p=0.03). After 6 months of insulin treatment BMI was 30.3+/-4.2 kg/m2 (p<0.05), mean weight increase was 2.7+/-0.8 kg. M-value was substantially increased to 4.5+/-2.3 mg kg-1 min-1 (p<0.001), the degree of improvement depended on basal insulin sensitivity (r=-0.55, p<0.01). HbA1c was reduced to 7.7+/-1.4% (p<0.01), the correlation M-value with change of HbA1c (r=-0.59, p<0.01) was shown. Total cholesterol decreased from 6.3+/-1.1 to 5.4+/-1.1 mmol/l, LDL-cholesterol from 4.1+/-1.1 to 3.4+/-1.0 mmol/l, triglycerides from 2.6+/-1.6 to 1.6+/-0.7 mmol/l (p<0.001). In conclusion, insulin treatment of type 2 diabetes patients leads to decrease in insulin resistance due to reduction in glucose toxicity and plasma atherogenicity despite weight gain.     

The renal metabolism of insulin: urinary insulin excretion in patients with mutant insulin syndrome (insulin Wakayama)

Many studies have shown that the kidney plays an important role in the metabolism of many proteins and small peptides. To understand insulin handling in the kidney, we examined urinary insulin excretion under several conditions in patients with mutant insulin syndrome (MIS; insulin Wakayama). Urinary excretion of insulin was studied using high-performance liquid chromatography analysis in patients with MIS. In these patients, most of the insulin extracted from a 24-hour urine collection and from urine collected after stimulation of insulin secretion by glucose or glucagon was normal insulin, whereas 90% of serum insulin is structurally abnormal (Leu-A3 insulin). On the other hand, arginine, which is known as an inhibitor of renal tubular reabsorption, increased urinary excretion of Leu-A3 insulin. The ratio of Leu-A3 and normal insulin in urine after arginine was similar to that in serum. A large amount of Leu-A3 insulin is excreted in urine when reabsorption of insulin at renal tubules is inhibited by arginine. These data indicate that normal and Leu-A3 insulin are filtered through the glomerulus with relatively little restriction. Using the fact that basal urine has a high concentration of normal insulin and an extremely low concentration of Leu-A3 insulin, which has less receptor-binding affinity, we speculated some possibilities. One possibility is that both forms of insulin are reabsorbed by the tubular cells, but with different efficiencies. Leu-A3 insulin absorption in more complete, and this suggests differences in the uptake pathways that may account for the differences in response to arginine infusions. Another possibility is that only normal insulin is secreted from tubules into urine which is mediated by receptors. Our results provide new insight into renal metabolism of insulin and showed that MIS is a useful model for studying it.