门冬胰岛素联合甘精胰岛素治疗2型糖尿病的疗效观察

目的探讨三餐前门冬胰岛素联合甘精胰岛素对血糖控制较差的糖尿病患者的疗效。方法选择血糖控制较差的糖尿病患者60例,随机分为两组：一组以三餐前门冬胰岛素联合睡前甘精胰岛素治疗（Asp＋Gla组）,另一组以三餐前诺和灵R联合睡前诺和灵N治疗（RI＋NPH组）。比较两组治疗后血糖达标时间、FBG、2hBG、血糖波动、胰岛素用量、低血糖发生率。结果Asp＋Gla组降糖快速稳定,血糖达标时间短,治疗后FBG、2hBG更理想,日内血糖波动幅度小,低血糖发生率低,优于RI＋NPH组（P均〈0．05）。结论对血糖控制较差的2型糖尿病患者,三餐前门冬胰岛素联合睡前甘精胰岛素治疗,低血糖发生率低,降糖效果显著。     

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.     

地特胰岛素与甘精胰岛素治疗2型糖尿病的临床效果比较

目的比较地特胰岛素(Det)与甘精胰岛素(Gla)联合速效胰岛素治疗T2DM疗效。方法将血糖控制不佳T2DM患者70例分为Det组和Gla组,每组35例,治疗24周,比较两组治疗前后HbAl c、FPG、晚餐前血糖(PDPG)、胰岛素剂量、体重增加及低血糖发生情况。结果经过24周治疗,两组HbA1c、FPG均下降(P0.01),组间比较差异无统计学意义。两组PDPG均下降(P0.01),组间比较差异有统计学意义(P0.01)。Gla组胰岛素剂量较Det组低,体重增加较Det组高(P0.05)。Det、Gla组低血糖事件发生风险分别为8.69、8.92事件/(患者·年)。结论 1次/d Det联合速效胰岛素是治疗血糖控制不佳T2DM患者的有效方案之一。     

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.     

达格列净联合甘精胰岛素及门冬胰岛素对2型糖尿病血糖控制不佳患者血糖波动的影响

目的探讨达格列净联合甘精胰岛素及门冬胰岛素对2型糖尿病血糖控制不佳患者血糖波动的影响。方法 56例血糖控制不佳的2型糖尿病患者[糖化血红蛋白(HbA1c)7%]随机分成达格列净组和对照组各28例。所有患者入院后停用之前降糖药物,给予生活方式干预,对照组给予甘精胰岛素联合门冬胰岛素治疗,达格列净组在对照组基础上给予达格列净10 mg/d,早餐前口服。监测两组每日三餐前后及夜间1点的血糖,并根据监测结果调整胰岛素用量,空腹血糖7 mmol/L、餐后2 h血糖10 mmol/L认定为血糖达标。比较两组入院后第2天及治疗1 w后平均血糖(MBG)、血糖水平标准差(SDBG)、最大血糖波动幅度(LAGE)、餐后血糖波动幅度(PPGE),并统计治疗期间低血糖发生次数。结果 (1)两组基线资料比较差异均无统计学意义(P0.05);(2)治疗1 w后,两组各时点血糖及血糖波动指标与治疗前比较均显著降低(P0.05);(3)治疗后,达格列净组血糖波动指标及胰岛素用量均明显优于对照组(P0.05)。两组治疗前后均无低血糖事件。结论较单用胰岛素治疗,达格列净联合甘精及门冬胰岛素能进一步降低血糖水平,同时可显著降低日内及日间血糖波动,减少胰岛素用量,并不增加低血糖风险。     

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。     

一天一次地特胰岛素控制空腹血糖的疗效和安全性评价

FPG对糖尿病患者整体血糖水平和心脑血管糖尿病并发症的防治都至关重要。地特胰岛素（Det）是一种长效基础胰岛素,降糖作用持久且平稳。一天一次Det能有效控制FPG,还能降低治疗中的个体变异性。与中效人胰岛素和长效甘精胰岛素（Gla）相比,Det治疗的患者有较低的低血糖发生率和较少的体重增加。鉴于其优良的疗效和安全性,一天一次Det治疗不受体重和年龄的限制,适应证广泛,是控制FPG的理想选择。     

动态血糖监测与胰岛素泵在围手术期糖尿病患者的应用

将52例围术期糖尿病患者随机分为2组:I组患者采用动态血糖监测系统与胰岛素泵联合监测治疗模式(CGM+CSII),II组采用单纯胰岛素泵治疗(CSII),该组患者监测其指端血糖;比较2组治疗3d后的血糖控制情况、血糖达标率、平均血糖(MBG)、平均血糖波动幅度(MAGEl及低血糖发生次数)。结果:治疗3d后CGMS+CSII和CSII两组患者的空腹血糖、3餐后血糖、晚23:0血糖及凌晨3:00血糖均明显低于治疗前(P<0.05),血糖达标率分别为79%和64%,胰岛素泵治疗3d后患者的MBG和MAGE较治疗前均明显下降(P<0.05)。其中CGMS十CSII组患者的MBG、MAGE均显著低于CSII组(P<0.05);胰岛素治疗前CGM+CSII组患者1 d发现低血糖次数多于CSII组(P<0.05);治疗3d后CGM组患者的低血糖次数低于治疗前(P<0.05),而CSII组患者的低血糖次数高于治疗前(P<0.05)。结论:动态血糖检测系统能全面提供血糖水平的信息,及时发现和减少血糖波动及低血糖反应,与胰岛素泵在临床上联合应用更有利于糖尿病患者围术期中的血糖控制达标。     

甘精胰岛素联合沙格列汀或格列美脲对2型糖尿病血糖波动的影响

选择2015年1~12月142例T2DM患者,随机分为对照组(71例)应用甘精胰岛素+格列美脲,观察组(71例)应用甘精胰岛素+沙格列汀。结果治疗后两组FPG、HbA_(1c)及胰岛素用量对比(P0.05);治疗后观察组血糖标准差(SDBG)、日内血糖平均波动幅度(MAGE)、日间血糖平均绝对差(MODD)水平均优于对照组(P0.05);两组低血糖AUC水平对比(P0.05)。结论甘精胰岛素与沙格列汀联合可有效改善患者血糖水平,降低患者血糖波动幅度。     

甘舒霖R联合甘精胰岛素治疗脆性糖尿病

将24例脆性糖尿病患者随机分为应用阿卡波糖联合甘精胰岛素治疗(对照组)12例、应用甘精胰岛素联合甘舒霖R治疗(治疗组)12例,观察两组患者治疗后两周内低血糖相关指标和其他血糖波动参数,包括低血糖发生率(PT3.9,即血糖低于3.9 mmol/L的时间比)、低血糖发生次数、高血糖发生率(PT7.8、PT11.1,即血糖高于7.8 mmol/L或11.1mmol/L的时间比)、血糖波动系数(即连续测定的血糖值标准差,SDBG)最大血糖波动幅度(LAGE)和平均血糖波动幅度(MAGE),3月后比较两组患者上述参数及糖化血红蛋白的水平。结果对照组PT7.8[(21.85±11.43)%]、PT11.1[(35.54±12.1)%]、SDBG(4.34±0.94)、LAGE[(13.21±1.82)mmol/L]、MAGE[(10.5±1.37)mmol/L]和HbA_(1C)(%)[(8.5.±2.1)%]等指标均高于治疗组(54.56±12.56)%、(19.45±10.5)%、(2.81±1.12)、(10.13±2.31)mmol/L、(7.4±1.45)mmol/L]、[(6.4±1.1)%]的糖尿病患者。差异均有高度统计学意义(均P0.01)。对照组的PT3.9[(10.13±2.4)%]和治疗组的[(12.57±3.5)%]结果相似,无统计学意义(P0.05)。结论甘精胰岛素联合阿卡波糖难以平稳控制脆性糖尿病患者血糖水平,应用甘精胰岛素联合甘舒霖R可以有效控制全天血糖。     

糖调节受损个体胰岛β细胞功能和胰岛素抵抗观察

评价152例人选者[正常糖耐量、空腹血糖受损和(或)糖耐量受损]胰岛β细胞功能和胰岛素抵抗.结果 显示空腹血糖受损者主要表现胰岛素早期分泌功能缺陷和基础分泌不足,胰岛素抵抗严重;糖耐量受损者则胰岛素早期和晚期分泌功能显著下降伴轻度胰岛素抵抗.     

Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose tolerance

OBJECTIVE: This study was designed to evaluate the effects of rosiglitazone (ROS) on insulin sensitivity, beta-cell function, and glycaemic response to glucose challenge and meal in subjects with impaired glucose tolerance (IGT). METHODS: Thirty patients with IGT (ages between 30 and 75 years and BMI (body mass index) < or = 27 kg/m2) were randomly assigned to receive either placebo (n = 15) or ROS (4 mg/day) (n = 15). All participants underwent a 75-g oral glucose tolerance test (OGTT), meal test, and frequently sampled intravenous glucose tolerance test (FSIGT) before and after the 12-week treatment. RESULTS: After 12 weeks of ROS treatment, there were significant increases in total cholesterol (TC) (4.25 +/- 0.22 vs 4.80 +/- 0.17 mmol/l, P < 0.001), high-density lipoprotein cholesterol (HDL-C) (1.25 +/- 0.07 vs 1.43 +/- 0.06 mmol/l, P < 0.05), and low-density lipoprotein cholesterol (LDL-C) (2.70 +/- 0.15 vs 3.37 +/- 0.17 mmol/l, P < 0.05) without changes in triglyceride concentration, TC/HDL-C and LDL-C/HDL-C ratio. Although the acute insulin response (AIR) to intravenous glucose and disposition index (measured as the ability of pancreatic beta-cell compensation in the presence of insulin resistance) remained unchanged, the insulin sensitivity (SI) and glucose effectiveness (SG) were remarkably elevated (0.38 +/- 0.06 vs 0.54 +/- 0.09 x 10(-5) min(-1)/pmol, P < 0.05; 0.017 +/- 0.002 vs 0.021 +/- 0.001 min(-1), P < 0.05, respectively) in the ROS group. The glucose, insulin, and c-peptide areas under curve (AUC) in response to OGTT and the glucose and insulin AUC during meal were significantly ameliorated in the ROS group. Five out of 15 (33%) and two out of 15 (13%) subjects treated with ROS and placebo, respectively, reversed to normal response during OGTT (P < 0.05). CONCLUSION: Rosiglitazone treatment significantly improved insulin resistance and reduced postchallenge glucose and insulin concentrations in patients with impaired glucose tolerance without remarkable effects on beta-cell secretory function.     

Usefulness of plasma glucose and insulin concentrations in identifying patients with insulin resistance

In this study, a specific measurement of insulin-mediated glucose disposal was used in 490 healthy volunteers to classify subjects as being insulin resistant. We then made standard measurements of plasma glucose and insulin concentrations to see how useful they would be as surrogate markers of insulin resistance.     

空腹血糖异常人群胰岛素分泌功能及胰岛素抵抗状态的探讨

目的　探讨空腹血糖异常人群的胰岛素分泌及胰岛素抵抗状态。　方法　选择包钢糖尿病普查中复查口服葡萄糖耐量试验 (OGTT) 3985例 ,分为 6组 :正常糖耐量 (NGT)组 2 5 88例 ,异常空腹血糖 (IFG)组 2 72例 ,糖耐量减低 (IGT)组 4 4 9例 ,空腹血糖异常伴糖耐量减低 (IFG/ IGT)组116例 ,新诊断糖尿病 (DM1)组 338例 ,已知糖尿病 (DM2 )组 2 2 2例。测腰围、体重指数、血压、血脂及血浆胰岛素 ,应用稳态模式胰岛素抵抗指数 (HOMA- IR)作为胰岛素抵抗指标 ,稳态模式胰岛 β细胞功能指数 (HBCI)及胰岛素分泌指数 (IS)作为胰岛素分泌指标 ,并对 6组患者的这些指标及临床特征 ,进行对比分析。　结果　与 NGT组比较 ,IFG组 HOMA- IR(1.4 6± 0 .6 0 ,1.0 6± 0 .6 4 ,t=- 6 .716 ,P<0 .0 0 1)、空腹胰岛素 (FINS) (17.90± 10 .0 6 ,15 .79± 10 .94 ,t=- 2 .0 71,P=0 .0 39)增高 ,HB-CI(4.6 5± 0 .6 0 ,5 .2 7± 0 .76 ,t=3.399,P<0 .0 0 1)及 IS(0 .86± 0 .6 0 ,0 .99± 0 .6 2 ,t=2 .36 6 ,p=0 .0 18)降低 ;IGT组 HOMA- IR(1.39± 0 .5 8,t=4 .6 98) ,FINS(2 1.2 7± 15 .39,t=4 .4 93)、2 - h胰岛素(6 0 .84± 37.86 ,t=8.4 82 )、HBCI(5 .4 7± 0 .79,t=2 .6 98)、IS(1.2 5± 0 .6 1,t=4 .0 34,P值均 <0     

正常糖耐量者口服葡萄糖-胰岛素释放试验的胰岛素分泌曲线特点的研究

目的研究口服葡萄糖一胰岛素释放试验（OGIRT）的胰岛素（Ins）分泌曲线特点,初步探讨适用于I临床评价个体胰岛素敏感性和8细胞分泌功能的方法。方法对12例正常糖耐量者行OGIRT和静脉糖耐量试验（IVGTT）,观察OGIRT、IVGTT血浆Ins分泌峰值时间分布频数,分析胰岛素敏感性和B细胞功能各指标相关指数。结果OGIRT血浆Ins分泌高峰出现于35-45min,无明显第二分泌峰。经多因素线性回归分析表明20、30、35minIns增值与葡萄糖增值的比值（ΔI20／ΔG20、ΔI30／ΔG30、ΔI35／ΔG35）与第一相（1PH）胰岛素分泌、葡萄糖及胰岛素曲线下面积比值（SGI）、胰岛素作用指数（IAI）、HOMA—IR、胰岛素分泌指数均不相关（P〉0．05）,ΔI40／ΔG40与SGI、IAI、HOMA-IR显著相关（P均〈0．01）。结论OGIRT可能不能反映1PH;OGIRTΔI40／ΔG40比I20／ΔG20、△I30／ΔG30能更好地评估β细胞功能。     

Relationship between glucose tolerance,insulin secretion,and insulin action in non-obese individuals with varying degrees of glucose tolerance

Summary Plasma glucose and insulin concentration following a 75 g oral glucose challenge and glucose uptake during a hyperinsulinaemic glucose clamp study were determined in 50 non-obese individuals. The study population was divided into five groups on the basis of their glucose tolerance: normal, impaired glucose tolerance, Type 2 (non-insulin-dependent) diabetes mellitus with fasting plasma glucose of less than 8 mmol/l, between 8–15 mmol/l, and more than 15 mmol/l. The plasma insulin response was significantly greater (p<0.001) than normal in those with either impaired glucose tolerance or Type 2 diabetes and a fasting plasma glucose concentration less than 8 mmol/l. In contrast, the plasma insulin response was similar to normal in the other two groups of patients with Type 2 diabetes, i.e. fasting plasma glucose concentration 8–15 mmol/l or greater than 15 mmol/l. Glucose uptake rates were significantly lower (p<0.001) than normal in subjects with impaired glucose tolerance and all three groups of patients with Type 2 diabetes. Although glucose uptake rates during the glucose clamp studies were relatively similar in all four groups of glucose intolerant subjects, the values were significantly lower in those patients with Type 2 diabetes who had a fasting plasma glucose concentration greater than 8 mmol/l (p<0.01), These data indicate that a significant degree of insulin resistance exists in patients with impaired glucose tolerance or Type 2 diabetes, relatively independent of fasting plasma glucose concentration. Indeed, glucose uptake during glucose clamp studies fell 8-fold over a range in fasting plasma glucose concentration of from 4.5 to 6.5 mmol/l. In contrast, the plasma insulin response increased over the same range of fasting plasma glucose concentrations. The fact that this defect in insulin action can be seen in patients who are hyperinsulinaemic, not hypoinsulinaemic, and only modestly hyperglycaemic, is consistent with the hypothesis that resistance to insulin-stimulate glucose uptake is a basic characteristic of patients with impaired glucose tolerance or Type 2 diabetes.     

Disordered glucose and insulin metabolism in patients with insulinoma.

The response of plasma glucose and insulin to infusion of glucose and of epinephrine plus propranolol were examined in normal subjects and in two patients with surgically proven insulin-secreting islet cell tumors. The plasma immunoreactive insulin concentration in the two patients was both inappropriate and independent of the plasma glucose concentration. Their insulin secretion was neither increased by physiologic stimulants nor decreased by pharmacologic inhibitors of insulin secretion. There are diagnostic uses for these data as well as theoretical implications. We propose a physiological approach to establish the diagnosis of insulin-secreting islet cell tumors.     

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose

Our laboratory is interested in the metabolic effects of ingested proteins. As part of this research, we currently are investigating the metabolic effects of ingested individual amino acids. The objective of the current study was to determine whether leucine stimulates insulin and/or glucagon secretion and whether, when it is ingested with glucose, it modifies the glucose, insulin, or glucagon response. Thirteen healthy subjects (6 men and 7 women) were studied on 4 different occasions. Subjects were admitted to the special diagnostic and treatment unit after a 12-hour fast. They received test meals at 8:00 am. On the first occasion, they received water only. Thereafter, they received 25 g glucose or 1 mmol/kg lean body mass leucine or 1 mmol/kg lean body mass leucine plus 25 g glucose in random order. Serum leucine, glucose, insulin, glucagon, and α-amino nitrogen concentrations were measured at various times during a 2.5-hour period after ingestion of the test meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that approximately present in a 350-g steak. After leucine ingestion, the leucine concentration increased 7-fold; and the α-amino nitrogen concentration increased by 16%. Ingested leucine did not affect the serum glucose concentration. When leucine was ingested with glucose, it reduced the 2.5-hour glucose area response by 50%. Leucine, when ingested alone, increased the serum insulin area response modestly. However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the response. Ingested leucine stimulated an increase in glucagon. Ingested glucose decreased it. When ingested together, the net effect was essentially no change in glucagon area. In summary, leucine at a dose equivalent to that present in a high-protein meal, had little effect on serum glucose or insulin concentrations but did increase the glucagon concentration. When leucine was ingested with glucose, it attenuated the serum glucose response and strongly stimulated additional insulin secretion. Leucine also attenuated the decrease in glucagon expected when glucose alone is ingested. The data suggest that a rise in glucose concentration is necessary for leucine to stimulate significant insulin secretion. This in turn reduces the glucose response to ingested glucose.     

Plasma glucose and insulin responses to oral glucose in nonobese subjects and patients with endogenous hypertriglyceridemia

Plasma glucose and insulin responses to a 50-gm oral glucose challenge were determined in 396 nonobese subjects: 220 patients with endogenous hypertriglyceridemia and 176 normal persons. These groups were further subdivided on the basis of relative body weight: 1.0-1.1 and 1.1-1.2. Patients with endogenous hypertriglyceridemia whose obesity index was between 1.0 and 1.1 had significantly increased plasma glucose (more than 25%, P less than 0.001) and insulin (more than 18%, P less than 0.01) responses. Similar findings were also observed in patients with endogenous hypertriglyceridemia whose index of obesity was between 1.1 and 1.2, ie, there was a 25% increase in the plasma glucose response (P less than 0.001) and a 37% increase in the plasma insulin response (P less than 0.001). Thus, endogenous hypertriglyceridemia can occur in nonobese individuals, and these patients have an increase in their plasma glucose and insulin responses when weight-matched with nonobese normal subjects.