罗格列酮治疗以餐后低血糖反应为首发症状2型糖尿病研究

36例患者按（2：1）随机分为,对照组（n=12）,罗格列酮组（n=24）;对照组予改善生活方式;罗格列酮组予改善生活方式和罗格列酮4mg／日,结果经12周治疗后,对照组空腹及负荷后血糖及胰岛素与治疗前相比无明显统计学差异（P均〉0．05）;罗格列酮组治疗后空腹及负荷后血糖及胰岛素与治疗前及对照组治疗后相比明显下降（P均〈0．05）;治疗后对照组体重及BMI较治疗前下降（P〈0．05）;罗格列酮组体重及BMI与治疗前相比无明显变化（P〉0．05）;治疗前后对照组ISI较治疗前无明显变化;罗格列酮组ISI较治疗前明显升高（P〈0．05）,低血糖症状消失。结论对于以餐后低血糖反应为首发症状的T2DM患者,罗格列酮增加胰岛素敏感性,减轻餐后低血糖反应的发生。     

罗格列酮联合其它降糖药治疗2型糖尿病的观察

将120例2型糖尿病患者分成对照组60例继续使用合适剂量的磺脲类、二甲双胍、磺脲类＋二甲双胍、胰岛素；治疗组60例在使用原剂量药基础上加服罗格列酮（文迪雅）4mg／d共用三个月，，观察前后空腹血糖（FPC）、餐后血糖（PpG）、糖化血红蛋白（HbA1c）、空腹胰岛素（FINS）、血甘油三脂（TG）、高密度蛋白质（HDL）、低密度蛋白质（LDL）、体重指数（BMI）以及胰岛素敏感指数（ISI）。结果治疗组治疗后FPG、PPG、HbA1c、FINS、TG、LDL均有明显下降，HDL、ISI显著上升（P〈0．05）；对照组治疗前后上述指标均无明显改变（P〉0．05）。结论 胰岛素增敏剂罗格列酮能安全有效地改善血糖水平，提高胰岛素敏感指数，降低胰岛素抵抗，改善胰岛B细胞分泌功能。     

罗格列酮对2型糖尿病合并高血压患者血压的作用

目的：运用胰岛素增敏剂罗格列酮治疗2型糖尿病伴高血压患者，研究其降压作用及降压机理。方法：38例2型糖尿病伴高血压患者，口服罗格列酮（文迪雅）4～8mg／d，共12周，观察治疗前后的血压、瘦素、血糖和胰岛素水平，计算胰岛素敏感指数和胰岛素抵抗指数，并进行分析比较。结果：罗格列酮治疗后收缩压和舒张压明显下降（P〈0．05）；甘油三酯（TG）、空腹血糖（FBG）、餐后血糖（PBG）、空腹胰岛素（FINS）和餐后胰岛素（PINS）均明显降低（P均〈0．05）；瘦素水平明显升高（P〈0．01）；胰岛素敏感性指数（ISI）显著升高（P〈0．05），胰岛素抵抗指数（IR）显著下降（P〈0．05）。结论：罗格列酮在降低血糖、改善胰岛索抵抗、提高胰岛素敏感指数的同时，具有升高瘦素水平和降低血压的作用。     

罗格列酮对IGT患者脂餐后糖、脂代谢的影响

将32例葡萄糖耐量减低（IGT）患者根据胰岛素抵抗指数（IR）分为A、B两组各16例,IR分别〉2、≤2;两组空腹、餐后血糖（BG）及糖化血红蛋白（HbA1c）、体重指数（BMI）无显著差异（P〉0．05）。观察罗格列酮对两组脂肪餐后血糖（BG）、胰岛素（INS）、血脂变化。结果A组顿服罗格列酮8mg餐后4h内BG、游离脂肪酸、甘油三酯及低密度脂蛋白水平显著降低（P均〈0．05）,而INS无显著变化;B组未见显著改变。认为8mg罗格列酮顿服对胰岛素抵抗的IGT患者有明显的胰岛素增敏作用,其机制是通过直接或间接促进甘油三酯的清除或利用实现的。     

罗格列酮和还原型谷胱甘肽治疗非酒精性脂肪肝患者疗效观察

目的观察罗格列酮和还原型谷胱甘肽对非酒精性脂肪肝患者的临床治疗效果,并探讨可能的作用机制.方法将84例非酒精性脂肪肝患者随机分为对照组、罗格列酮治疗组、还原型谷胱甘肽治疗组及罗格列酮和还原型谷胱甘肽联合治疗组.四组患者均进行饮食控制及适当的运动.治疗组分别给予罗格列酮、还原型谷胱甘肽及两药联合治疗8周,测定腰围、体重指数（BMI）;常规检测血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、甘油三酯、总胆固醇、空腹血糖（FBG）、空腹胰岛素（FINS）、肿瘤坏死因子-α（TNF-α）及胰岛素抵抗指数（HOMA-IR）.结果罗格列酮组和联合治疗组患者腰围、BMI较对照组及还原型谷胱甘肽组明显改善（腰围,F=8.11,P=0.001;BMI,F=7.78,P=0.001）;与对照组比,三个治疗组患者血清TG、TC无明显改善（TG,F=0.81,P=0.49;TC,F=0.39, P=0.76）,还原型谷胱甘肽组ALT、AST较对照组均明显改善（P=0.001）,罗格列酮治疗组及联合治疗组患者ALT、AST、TNF-α及 HOMA-IR 较对照组均明显改善（ALT,F=7.11,P=0.002;AST,F=9.14,P=0.001;TNF-α, F=6.98,P=0.002;HOMA-IR,F=7.995,P=0.001）.结论罗格列酮和还原性谷胱甘肽可促进非酒精性脂肪肝患者肝功能的恢复,并且罗格列酮对患者胰岛素抵抗状态有显著的改善作用.     

二甲双胍联用罗格列酮治疗2型糖尿病疗效观察

目的了解二甲双胍联用罗格列酮（RGZ）治疗2型糖尿病（T2DM）的疗效及优点。方法将53例T2DM患者随机分为二甲双胍联用格列吡嗪组（A组）、二甲双胍联用RGZ组（B组），进行6个月治疗，测定治疗前后BP、PG、BMI、HbA，C、Ins、血脂等指标，并计算胰岛素抵抗指数（HOMA-IR）。结果两组治疗均可使BP、PG、BMI、HbA1c及LDL-C下降（P〈0．05），但B组同时可使Ins水平下降（P〈0．05）、HOMA-IR降低（P〈0．01）。结论二甲双胍联用RGZ可改善T2DM患者的糖脂代谢紊乱，并降压、减重，同时改善IR。     

罗格列酮与胰岛素治疗对2型糖尿病患者胰岛β细胞第一时相分泌功能的影响

目的罗格列酮（RGZ）与胰岛素治疗对2型糖尿病（T2DM）患者胰岛功能的影响。方法FPG）11．1mmol／L的患者随机分为胰岛素治疗（Ins）组和胰岛素＋罗格列酮治疗（Ins＋RGZ）组,两组年龄、病程、BMI均无统计学差异。血糖达标后再维持治疗3个月。治疗前后均作静脉糖耐量试验（IVGTT）,比较两组糖代谢和胰岛功能的变化。结果治疗后的FPG、2hPG、HbA1c、静脉葡萄糖曲线下面积（AUC-G0～60）均显著下降,HOMA—B改善（P〈0．01或P〈0．05）,两组间无统计学差异。两组IVGTT10min内胰岛素释放曲线下面积／60min内胰岛素释放曲线下面积（AUC-I0～10／AUC-I0～60）分别增加10％和12％（P=0．085,0．05）。Ins＋RGZ组I2、I5、I10及FC-P显著提高,Ins组增高无统计学意义。逐步回归分析显示,治疗后FPG和2hPG下降与负荷后胰岛素增值和血糖增值比值呈正相关（r=0．593,P=0．000;r=0．548,P=0．001）,表明治疗后胰岛素处理葡萄糖能力与血糖控制程度呈正相关。结论罗格列酮（而不是胰岛素）能恢复第一时相胰岛素分泌。T2DM患者早期联用RGZ,有利于保护胰岛β细胞功能。     

盐酸罗格列酮对2型糖尿病合并高血压患者血压的影响

目的运用胰岛素增敏剂盐酸罗格列酮治疗2型糖尿病伴高血压患者，研究其降压作用和降压机理。方法30例2型糖尿病伴高血压患者口服盐酸罗格列酮（维戈洛）4mg／d-8mg／d，共16周，观察治疗前后的血压、血脂、血糖和胰岛素水平，计算胰岛素敏感指数和胰岛素抵抗指数，并进行分析比较。结果盐酸罗格列酮治疗后收缩压和舒张压明显下降（P〈0．01）；空腹血糖（FBG）、餐后血糖（PBG）、空腹胰岛素（FINS）和餐后胰岛素（PINS）均明显降低（P〈0．01）；胰岛素敏感指数（ISI）显著升高（P〈0．01），胰岛素抵抗指数（IR）显著下降（P〈0．05）。结论盐酸罗格列酮在降低血糖、改善胰岛素抵抗、提高胰岛素敏感指数的同时，具有降低血压、血脂的作用，且安全性和耐受性均较好。     

评估胰岛素分泌及胰岛素敏感性选择降糖药物的临床多中心研究

目的评价糖尿病病理生理变化对新诊断的2型糖尿病患者治疗的指导意义。方法按照精氨酸刺激试验的结果，将322例新诊断2型糖尿病患者分为一相胰岛素分泌正常组和低下组，将前者随机分配至瑞格列奈、罗格列酮及二甲双胍治疗组，后者随机分配至瑞格列奈、罗格列酮及格列吡嗪治疗组。结果（1）各药物治疗组，用药后3个月、6个月的空腹血糖、餐后2h血糖及HbA1C均较基线明显降低（均P〈0．01）。治疗后6个月HbA1C控制理想的总体达标率为63．5％。（2）在一相胰岛素分泌正常组，罗格列酮治疗后血糖校正后的精氨酸试验胰岛素曲线下面积（AUC）明显增加，胰岛素原显著减少（P〈0．01），二甲双胍治疗后胰岛素抵抗指数（HOMA—IR）较基线显著降低（P〈0．05）。（3）在一相胰岛素分泌低下组，瑞格列奈或格列吡嗪治疗后的精氨酸试验的2、4、6min真胰岛素均值与空腹真胰岛素的差值（△TI）、血糖校正后精氨酸试验的结果（ATI／PG）、AUC及真胰岛素（TI）明显增高（P〈0．05或P〈0．01），罗格列酮组治疗后的ATI／PG与AUC显著增加，而HOMA—IR及胰岛素原较治疗前明显减少（均P〈0．01）。结论（1）基于糖尿病病理生理变化正确评估的药物治疗，可有效控制新诊断2型糖尿病患者的糖代谢紊乱。（2）瑞格列奈及格列吡嗪可增加2型糖尿病患者的一相胰岛素分泌及真胰岛素水平。（3）罗格列酮不仅可以增加机体的胰岛素敏感性，减少胰岛素原的分泌，尚可改善一相胰岛素分泌低下者的一相胰岛素分泌功能。（4）新诊断2型糖尿病患者血糖的有效控制，主要与机体胰岛素分泌功能的改善及胰岛素敏感性的增加有关。     

胰岛素抵抗与高血压病关系流行病学研究

目的：探讨胰岛素抵抗与高血压病的相互关系。方法：采取整群随机抽样的方法抽取调查样本，选择徐州市大屯社区110位中年居民为调查对象，运用病例对照研究，测得血糖、胰岛素（INS）等浓度．求得胰岛素敏感指标（ISI）．并作统计学处理。结果：（1）高血压组（29例）中的空腹、负荷INS，高血压合并冠心病组（10例）中的空腹、负荷血糖，空腹、负荷INS明显高于对照组（71例），而空腹、负荷ISI低于对照组（P〈0．05）；（2）ISI与体重指数、收缩压、舒张压、血糖、甘油三酯、载脂蛋白B呈负相关（r=-0．603～-0．190，P〈0．05）；空腹、负荷ISI与高密度脂蛋呈正相关（r=0．391．0．193，P〈0．05）。结论：胰岛素抵抗是高血压病的重要危险因素。     

Thiazolidinediones increase hepatic insulin extraction in African Americans with impaired glucose tolerance and type 2 diabetes mellitus. A pilot study of rosiglitazone

Peripheral insulin levels are determined by beta-cell secretion, insulin sensitivity, and hepatic insulin extraction (HIE). We have previously shown that whereas sulfonylureas reduce insulin extraction, metformin enhances HIE. However, the effects of thiazolidinediones (TZDs) on HIE remain uncertain. Thus, we investigated the potential contribution of hepatic insulin clearance to peripheral insulin levels during rosiglitazone therapy in African Americans with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM). The study was composed of 12 first-degree relatives with IGT and 17 patients with newly diagnosed type 2 DM. Nineteen healthy relatives with normal glucose tolerance served as controls. Serum glucose, insulin, and C-peptide, and HIE (C-peptide-insulin molar ratios) were measured at t = 0 and 120 minutes during oral glucose tolerance test (OGTT) in all the subjects. The OGTT was performed before and after 3 months of rosiglitazone therapy (4 mg/d x 4 weeks and >8 mg/d x 8 weeks) in patients with IGT and type 2 DM. Insulin resistance index and beta-cell function were calculated in each subject using homeostasis model assessment (HOMA). Rosiglitazone therapy improved but did not normalize the overall glycemic control in the IGT and type 2 DM groups. After rosiglitazone therapy, the mean serum insulin and C-peptide levels at fasting remained unchanged. However, the 2-hour serum glucose and insulin were lower, whereas serum C-peptide was unchanged during 3 months of rosiglitazone treatment. Mean insulin resistance index of HOMA was reduced by 30% (4.12 +/- 1.95 vs 6.33 +/- 3.54, P < .05) in the type 2 DM group and by 21% (3.78 +/- 2.45 vs 4.81 +/- 3.49, P = NS) in the IGT group. Mean HIE values were significantly lower (70%) in the type 2 DM and IGT groups when compared with the normal glucose tolerance group. At 3 months, basal HIE was not significantly changed by rosiglitazone therapy in IGT and type 2 DM groups when compared with the baseline (0 month). However, rosiglitazone therapy was associated with increased HIE at 2 hours during OGTT by 40% and 30% in the IGT and type 2 DM groups, respectively, from the baseline (0 month) values. Furthermore, HIE inversely correlated with the insulin resistance index of HOMA (r = -.46, P < .05). We conclude that rosiglitazone therapy improved overall glucose tolerance and enhanced insulin sensitivity in patients with IGT and type 2 DM. Although basal HIE remained unchanged, rosiglitazone therapy increased postglucose challenge HIE in African Americans with IGT and type 2 DM. We speculate that TZDs increase insulin clearance or HIE after oral glucose challenge. This study suggests that in addition to insulin sensitization, rosiglitazone may be involved in insulin metabolism. The significance of the increased insulin clearance by TZD therapy remains uncertain and deserves further investigation in patients with insulin resistance and glucose intolerance.     

Rosiglitazone improves insulin sensitivity, glucose tolerance and ambulatory blood pressure in subjects with impaired glucose tolerance.

AIMS: To determine the effects of rosiglitazone on insulin sensitivity, glucose tolerance and ambulatory blood pressure when administered to subjects with persistent impaired glucose tolerance (IGT). METHODS: Eighteen subjects with persistent IGT were randomized to receive rosiglitazone 4 mg twice daily or matching placebo for 12 weeks. Evaluation at baseline and at the end of treatment included measurement of whole body insulin sensitivity during a euglycaemic hyperinsulinaemic clamp and deriving an insulin sensitivity index. Changes in glucose and insulin concentration were determined after oral glucose tolerance test (OGTT) and mixed meal tolerance tests, and 24-h ambulatory blood pressure was monitored. RESULTS: Rosiglitazone significantly improved the insulin sensitivity index by 2.26 micro g/kg per min per pmol/l relative to placebo (P = 0.0003). Four of nine subjects receiving rosiglitazone reverted to normal glucose tolerance and 5/9 remained IGT, although four of these had improved 2-h glucose values. In the placebo group, 1/9 subjects progressed to Type 2 diabetes and 8/9 remained IGT. Following OGTT and meal tolerance test, glucose and insulin area under curve were reduced over 3 and 4 h, respectively. Compared with placebo, ambulatory blood pressure decreased significantly in the rosiglitazone group by 10 mmHg systolic (P = 0.0066) and 8 mmHg diastolic (P = 0.0126). CONCLUSIONS: Consistent with its effects in patients with Type 2 diabetes, rosiglitazone substantially improved whole body insulin sensitivity and the glycaemic and insulinaemic responses to an OGTT and meal tolerance test in subjects with persistent IGT. Furthermore, rosiglitazone reduced systolic and diastolic ambulatory blood pressure in these subjects.     

罗格列酮联合减低体重对糖耐量受损患者的影响

糖耐量受损(IGT)患者治疗3个月后,单服罗格列酮患者血糖、胰岛素、稳态模型胰岛素抵抗指数(HOMA-IR)显著降低,同时减重治疗的患者上述指标降低程度优于单服罗格列酮患者.提示罗格列酮能改善IGT和胰岛素抵抗,如同时控制体重效果更佳.     

空腹血糖异常、糖耐量减低患者血清胰岛素水平的变化及其意义

目的 观察空腹血糖异常(IFG)、糖耐量减低(IGT)患者血清胰岛素水平的变化。方法 对50例空腹血糖和糖耐量正常者(NGT)、40例IFC和80例IGT患者行口服葡萄糖耐量试验(0GTT)，用氧化酶法检测血糖，用放免法测定血清空腹及餐后2小时胰岛素。结果 IFG、IGT组空腹血糖、空腹胰岛素水平及胰岛素敏感指数较NGT组明显升高(P＜0.05或P＜0．01)，IFG组胰岛素敏感指数与IGT组比较无显著性差异(P＞0．05)。结论 在IFG、IGT状态下已经存在胰岛素抵抗，而且在程度上两者间并没有显著性差异，应早期干预治疗。     

Effects of rosglitazone on plasma adiponectin, insulin sensitivity, and insulin secretion in high-risk African Americans with impaired glucose tolerance test and type 2 diabetes

We examined the metabolic effects of rosiglitazone therapy on glucose control, insulin sensitivity, insulin secretion, and adiponectin in first-degree relatives of African Americans with type 2 diabetes (DM) with impaired glucose tolerance (IGT) and DM for 3 months. The study was comprised of 12 first-degree relatives with IGT, 17 newly diagnosed DM, and 19 healthy relatives with normal glucose tolerance (NGT). Oral glucose tolerance test (OGTT) was performed before and after 3 months of rosiglitazone therapy (4 to 8 mg/d) in patients with IGT and DM. Serum glucose, insulin, C-peptide, and adiponectin levels were measured before and 2 hours during OGTT in the NGT and patients with IGT and DM. Insulin resistance index (HOMA-IR) and beta-cell function (HOMA-%B) were calculated in each subject using homeostasis model assessment (HOMA). Rosglitazone improved the overall glycemic control in the IGT and DM groups. Following rosiglitazone, the beta-cell secretion remained unchanged, while HOMR-IR was reduced in DM by 30% (4.12 +/- 1.95 v 6.33 +/- 3.54, P < .05) and the IGT group (3.78 +/- 2.45 v 4.81 +/- 3.49, P = not significant [NS]). Mean plasma adiponectin levels were significantly (P < .05) lower in the DM (6.74 +/- 1.95 microg/mL) when compared with the NGT group(9.61 +/- 5.09). Rosiglitazone significantly (P < .001) increased adiponectin levels by 2-fold in patients with IGT (22.2 +/- 10.97 microg/mL) and 2.5-fold greater in DM (15.68 +/- 8.23 microg/mL) at 3 months when compared with the 0 month. We conclude that adiponectin could play a significant role (1) in the pathogenesis of IGT and DM and (2) the beneficial metabolic effects of thiazolidinediones (TZDs) in high-risk African American patients.     

糖脉康对糖耐量减退者胰岛素敏感性的影响

目的了解糖脉康对糖耐量减退(IGT)者胰岛素敏感性的影响。方法将80例IGT患者随机分为对照组和治疗组,每组40例,在基础治疗的同时,对照组给予二甲双胍,治疗组给予糖脉康,观察两组治疗前后血糖、胰岛素、胰岛素敏感性指数(ISI)。结果两组治疗前后餐后血糖、空腹胰岛素、餐后胰岛素、ISI均较治疗前显著改善(P<0·01),两组间比较差别无显著性意义(P>0·05)。结论糖脉康可改善糖耐量减退患者的胰岛素敏感性。     

肥胖者胰岛素分泌功能对糖耐量低减及糖尿病发生的影响

目的　探讨肥胖者胰岛素分泌变化对糖耐量低减 (IGT)及糖尿病 (DM)发生的影响。　方法　对 30例单纯性肥胖 [体重指数 (BMI) >2 7]患者进行血糖和胰岛素测定 ,并观察胰岛细胞分泌指数 (HOMA- IS)及胰岛素敏感性指数 (IAI) ,并对这些患者进行 15年随访。　结果　肥胖者空腹胰岛素 (FINS)水平明显高于正常人 (P <0 .0 1) ,与 HOMA - IS明显的正相关 (P <0 .0 1) ;空腹血糖(FPG)与 HOMA- IS及 IAI呈明显的负相关 (P<0 .0 1)。15年内 6 3.3%的肥胖者发展成 IGT,5 0 .0 %的肥胖者及发展成 IGT者发展为 2型 DM。　结论　肥胖对 IGT及糖尿病的发生、发展有着明显的影响 ,控制体重是减少 IGT发生的重要环节。     

The effects of nateglinide following oral glucose load in impaired glucose tolerance subjects: rapid insulin stimulation by nateglinide in IGT subjects

This study was designed to determine the effect of a novel insulin secretagogue, nateglinide, on the glycemic response curve and early insulin secretion following oral glucose load in impaired glucose tolerance (IGT) subjects. Thirteen subjects were given a 75 g oral glucose tolerance test (75 g OGTT), the findings of which resulted in the diagnosis of IGT. The subjects returned to our hospital immediately. Eight subjects, in whom neither body weight nor life style (daily diet and exercise) was significantly altered during this period, were given 90 mg of nateglinide 5 min before a second oral glucose load in order to examine restoration of impaired early insulin secretion. Nateglinide administration resulted in the almost normalization of the glycemic response curve with restoration of impairment in early insulin response at 30 and 60 min after an oral glucose load. The area under the secreted insulin-time curve was not changed significantly by nateglinide administration. A single dose of nateglinide was shown to almost normalize the glycemic response curve after a 75 g OGTT and to restore impairment in early insulin response in IGT subjects.     

Exercise training but not rosiglitazone improves endothelial function in prediabetic patients with coronary disease

BACKGROUND: Impaired glucose tolerance (IGT) is associated with endothelial dysfunction and upregulation of inflammatory markers, which is potentially reversible by adequate treatment. It was our aim to compare the impact of exercise training with that of rosiglitazone on endothelial function and inflammatory markers in patients with IGT and coronary artery disease (CAD). METHODS: Patients with IGT and CAD were randomly assigned to either exercise training (n=13), rosiglitazone (8 mg; n=11), or a control group (n=10). During the first week, exercise training consisted of 6 x 15 min/d followed by three weeks of 30 min/d submaximal ergometer exercise. In addition, group exercise training of 1 h was performed twice per week. RESULTS: After 4 weeks, triglycerides and uric acid were significantly lower in the exercise group whereas fasting glucose, HbA1c, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, C-reactive protein, fibrinogen, and body mass index did not differ between groups. In the exercise group, exercise capacity (123+/-33 vs. 144+/-31 W; P=0.006) and endothelium-dependent, flow-mediated vasodilatation (P<0.01) increased significantly, whereas in the rosiglitazone group and in the control group (P=n.s.) no changes were seen. CONCLUSION: In patients with IGT and CAD, 4 weeks of exercise training exert significant and superior improvement of endothelium-dependent vasodilatation as compared with rosiglitazone therapy or usual care. This finding should be seen as an even further encouragement to recommend and, where available, prescribe exercise training to our patients.     

应用高葡萄糖钳夹技术评价糖耐量异常的Graves病患者胰岛β细胞功能及胰岛素抵抗

目的应用高葡萄糖钳夹技术评价糖耐量异常（IGT）的Graves病（GD）患者胰岛B细胞功能及胰岛素抵抗。方法筛选合并IGT的GD患者6例（均为初诊未治）,应用高葡萄糖钳夹技术检测胰岛素分泌及胰岛素敏感性,并与正常对照组10例进行比较,所有研究对象均检测谷氨酸脱羧酶（GAD）抗体。结果合并IGT的GD组与正常对照组比较,第一时相胰岛素分泌[（636．31±105．54）mIU／L比（233．56±21．33）mIU／L]、第二时相胰岛素分泌[（146．68±25．0）mIU／L比（67．06±6．23）mIU／L]、最大胰岛素分泌量[（195．05±32．94）mIU／L比（87．64±9．78）mIU／L],胰岛素敏感性指数（11．52±1．90比21．72±3．25）,差异均有统计学意义（P值均〈0．05）。所有研究对象GAD抗体检测均为阴性。结论GAD抗体阴性的GD合并IGT患者胰岛素分泌呈亢进状态,胰岛素敏感性显著低于正常对照组。