50克葡萄糖筛查阳性孕妇的前瞻性研究

目的比较妊娠糖尿病（GDM）及糖耐量减低（IGT）与糖耐量正常（NGT）孕妇的胰岛素敏感性（IS）及胰岛β细胞功能的差异，并寻找合理的评价指标，观察早期干预对妊娠结局的影响。方法比较313例NGT、128例IGT及270例GDM孕妇的临床特征，前瞻性研究糖负荷后的IS和β细胞功能，并对IGT及GDM组进行前瞻性干预。结果较NGT组升高。（2）IGT、GDM组较NGT组的（1）IGT及GDM组的孕前BMI、WBC、ALT等指标HOMA-IR、HOMA2-IR升高，△Ins60／△Glu60、IS-QUICKI及IS-OGTT则降低。（3）IGT及GDM组中除23例（5．8％）加用人胰岛素治疗外其余仅单纯饮食控制即可达标。分娩时其孕重增加较NGT组为少，且新生儿体重及巨大儿发生率与NGT组相当。结论胰岛素抵抗及β细胞功能代偿不足在GDM的发生中均起重要作用。评价孕期β细胞功能时，引入糖负荷后的指标可能更为准确。IGT及GDM孕妇经干预后巨大儿发生率可降低至正常孕妇水平。     

妊娠糖尿病患者血清瘦素水平与胰岛素抵抗的关系

28例妊娠糖尿病(GDM)患者和30例正常对照组(NGT)的研究显示，GDM组瘦素、空腹胰岛素、甘油三酯和胰岛素抵抗指数水平均比NGT组显著升高；瘦素和孕前BMI是影响GDM患者胰岛素抵抗的独立危险因子。     

不同糖耐量孕妇胰岛素抵抗和胰岛β细胞功能的变化

目的观察不同糖耐量孕妇胰岛素抵抗和胰岛β细胞功能变化。方法 248例孕妇于孕早期(孕5~12周)和孕中晚期(孕24~32周)检测空腹血糖(FPG)、空腹胰岛素(FINS),计算稳态模型胰岛素抵抗指数(HOMAIR)及胰岛β细胞分泌指数(HOMA-β);根据孕中晚期OGTT结果将孕妇分为妊娠期糖尿病组(GDM组)和无糖耐量受损组(NGT组),比较两组FPG、FINS、HOMA-IR及HOMA-β。结果 GDM组孕前BMI高于NGT组,P<0.05;两组年龄、采血孕周、新生儿体质量、巨大儿发生率比较,P均>0.05。与NGT组比较,GDM组孕早期FPG及孕中晚期FPG、HOMA-IR均升高,孕中晚期HOMA-β降低;与孕早期比较,GDM组孕中晚期FPG、HOMA-IR均升高(P均<0.05),NGT组孕中晚期FPG降低而FINS、HOMA-IR、HOMA-β升高(P均<0.05)。结论与NGT孕妇相比,GDM患者存在胰岛素抵抗和胰岛β细胞功能缺陷,孕中晚期表现更显著。     

胰岛素抵抗和胰岛β细胞分泌功能对妊娠糖尿病的影响

目的探讨胰岛素抵抗(IR)和β细胞分泌功能对妊娠糖尿病(GDM)的影响。方法观察妊娠中晚期孕妇糖耐量正常(NGT)者35例、糖耐量减低(IGT)者33例和GDM者38例在不同糖耐量状态下的IR和β细胞分泌功能,采用HOMA-IR和HOMA-β分别评价IR和β细胞分泌功能。结果IGT组的HOMA-IR明显高于NGT组(P<0·05),两组的HOMA-β的差异无统计学意义;GDM组的HOMA-IR明显高于NGT和IGT组(P<0·05),HOMA-β明显低于NGT和IGT组,差异均有统计学意义。结论妊娠中晚期孕妇IGT阶段胰岛素早期分泌功能受损,到GDM阶段兼有严重的IR和β细胞缺陷。从NGT、IGT到GDM,随着糖代谢紊乱的不断进展,IR逐渐加重,胰岛β细胞功能进行性减退。     

不同糖耐量状态孕妇的胰岛素敏感性与胰岛β细胞功能的研究

目的 评估不同糖耐量状态孕妇的胰岛素敏感性和胰岛β细胞功能的特点. 方法 GCT阳性受试者1561例,进一步行100g OGTT,其中正常糖耐量(NGT)651例,糖耐量减低(IGT)301例,妊娠糖尿病(GDM)609例.IGT组分为1小时血糖异常(1h-IGT)、2h或3h血糖异常(2/3h-IGT).用胰岛素敏感性指数ISI-Matsuda、HOMA-IR评估胰岛素敏感性,HOMA-β、1相和2相胰岛素分泌指数、胰岛素分泌敏感性指数(ISSI)评估胰岛β细胞功能. 结果 GDM组与IGT组年龄、TG水平显著高于NGT组(P均<0.01).从NGT组→IGT组→GDM组,ISI-Matsuda依次降低(P均<0.01);NGT组、IGT组HOAM-IR结果相近,显著低于GDM组(P均<0.01);各组HOMA-β差异无统计学意义(P>0.05);IGT组与NGT组1相、2相胰岛素分泌指数差异无统计学意义,均高于GDM组(P均<0.01);ISSI依次降低(P均<0.01).在IGT亚组中,1h-IGT组ISSI低于2/3h-IGT组. 结论 与NGT组比较,IGT组、GDM组临床特征无法区分.IGT组、GDM组胰岛素敏感性降低与胰岛β细胞功能障碍并存,且GDM组更加严重.与IGT其他亚组比较,1h-IGT状态更差.     

妊娠糖尿病患者胰岛素抵抗与血清C反应蛋白水平的相关性研究

目的:研究妊娠糖尿病(GDM)患者与正常妊娠妇女胎盘激素、超敏C反应蛋白(hs-CRP)与妊娠胰岛素抵抗和胰岛β细胞分泌功能的关系,分析发生GDM的危险因素,探讨GDM的发病机制.方法:GDM孕妇和正常孕妇各50例,均测胎盘激素、hs-CRP、血糖及胰岛素水平.结果:GDM组的hs-CRP水平明显高于正常对照组(P＜0.05).2组的胎盘激素水平(雌激素、孕激素、泌乳素)无统计学意义.GDM组的早期相胰岛β细胞分泌功能(△I30/△G30)明显低于对照组,P＜0.001.hs-CRP与孕前体重、孕前体重指数(BMI)、空腹胰岛素、稳态模式评估法胰岛素抵抗指数(HOMA-IR)呈正相关(r=0.287、0.289、0.248、0.299,P＜0.01),与△I30/△G30呈负相关(r=-0.509,P＜0.001).在纠正了孕前体重、孕前BMI、糖筛查时的体重和BMI后,hs-CRP与空腹胰岛素、HOMA-IR不再相关(P＞0.05).结论:炎症反应参与并加重妊娠胰岛素抵抗;GDM孕妇存在早期相胰岛β细胞分泌缺陷.     

妊娠期糖尿病胰岛素抵抗与铁蛋白和游离脂肪酸的相关性研究

目的探讨妊娠期糖尿病(GDM)孕妇胰岛素抵抗(IR)与铁蛋白(SF)和游离脂肪酸(FFA)的关系。方法 2011—2013年,按照随机原则选择在我院就诊的GDM孕妇71例为GDM组,正常孕妇50例为正常孕妇组,体检健康且未孕女性50例为正常非孕组。检测3组受试者血清SF、FFA、空腹血糖(FBG)及空腹胰岛素(Fins)水平,计算胰岛素抵抗指数(HOMA-IR)。结果正常非孕组、正常孕妇组及GDM组血清SF水平分别为(119.57±22.04)μg/L、(197.81±46.32)μg/L、(388.79±91.67)μg/L,差异有统计学意义(F=57.543,P0.01);GDM组血清SF水平高于正常孕妇组和正常非孕组,正常孕妇组高于正常非孕组(P0.01)。正常非孕组、正常孕妇组及GDM组血清FFA水平分别为(0.43±0.18)mmol/L、(0.67±0.14)mmol/L、(1.03±0.21)mmol/L,差异有统计学意义(F=37.619,P0.01);GDM组血清FFA水平高于正常孕妇组和正常非孕组,正常孕妇组高于正常非孕组(P0.01)。正常非孕组、正常孕妇组及GDM组HOMA-IR分别为(1.83±0.45)、(2.92±0.87)、(3.94±1.02),差异有统计学意义(F=45.071,P0.01);GDM组HOMA-IR高于正常孕妇组和正常非孕组,正常孕妇组高于正常非孕组(P0.01)。Pearson相关分析结果显示,血清SF水平(r=0.832)、血清FFA水平(r=0.759)均与HOMA-IR呈正相关(P0.01);血清SF水平与血清FFA水平呈正相关(r=0.893,P0.01)。结论 GDM孕妇存在IR及高铁蛋白血症、高游离脂肪酸血症,IR程度与血清SF、FFA水平相关,在GDM的早期干预中应重视SF和FFA的调控。     

妊娠糖尿病患者外周血白细胞核因子κB的表达

目的 了解妊娠糖尿病(GDM)患者外周血白细胞核因子κB(NF-κB)的表达情况.方法 随机入组正常孕妇(NGT组)、妊娠糖尿病孕妇(GDM组)、孕龄期未孕女性(Con组)各10例,以免疫荧光化学染色法和凝胶迁移电泳(EMSA)法检测外周血白细胞NF-κB的表达.结果 免疫荧光化学染色结果显示Con组细胞浆染色阳性,细胞核染色阴性;NGT组核内染色轻度阳性;GDM组核内染色显著阳性.EMSA结果显示GDM组、NGT组、Con组灰度相对百分比分别为28.32%、8.66%、5.71%,GDM组与Con组和NGT组间均有统计学差异(P<0.01),但Con组与NGT组间无统计学差异(P>0.05).结论 GDM患者白细胞核内NF-κB被激活,后者可能参与GDM的发病.     

妊娠糖尿病产后代谢综合征发病特点及影响因素研究

目的了解妊娠糖尿病(GDM)患者产后1年代谢综合征(MS)发病情况并分析影响因素。方法选择2009年1月至2012年6月于河北省沧州市中心医院GDM并于产后1年回访者126例(GDM组),选取同期分娩的糖代谢正常妇女并在产后1年应邀回访者114名为对照组(NGT组)。于孕中期收集孕前体重、糖尿病家族史、既往妊娠史等情况,并测量身高及体重,检测口服葡萄糖耐量试验(OGTT)各点血糖值、空腹胰岛素、空腹血脂,留置血清冰冻待测定高敏C反应蛋白(hs-CRP)。在产后1年进行随访,测量身高、体重、腹围、血压,检测空腹血糖、血脂。结果孕中期GDM患者较NGT组存在严重代谢紊乱,这种代谢紊乱在产后1年时仍持续存在;产后1年时GDM患者MS发病率为17.5%(22/126),对照组为7.9%(9/114)。Logistic回归分析显示产后发生MS的影响因素有OGTT时空腹血糖、孕前体重指数(BMI)、孕期hs-CRP及妊娠年龄,OR值分别为96.48、1.63、1.47及1.44。结论GDM患者产后MS发病率显著升高,其发生与孕期空腹血糖、孕前BMI、孕期hs-CRP及妊娠时年龄相关。     

妊娠期糖尿病血清肿瘤坏死因子-α、内脂素水平与胰岛素抵抗的相关性分析

采用稳态模型评估法评估正常糖耐量孕妇(NGT)、糖耐量减低孕妇(GIGT)和妊娠期糖尿病孕妇(GDM)的胰岛素抵抗指数,采用酶联免疫吸附法检测其血清TNF-α、内脂素及胰岛素水平。结果 GDM组和GIGT组HOMA-IR显著高于NGT组,GDM组HOMA-IR显著高于GIGT组。血清TNF-α、内脂素水平由NGT组到GIGT组和GDM组均呈显著增高,TNF-α、内脂素与空腹胰岛素、孕晚期体重指数、HOMA-IR均呈显著正相关。结论 TNF-α、内脂素水平与GDM患者IR程度密切相关,其水平可作为预测妊娠期糖尿病胰岛素敏感性的指标,将来可能是治疗妊娠期糖尿病的新靶点。     

门冬胰岛素与人胰岛素对妊娠合并糖代谢异常患者的有效性及安全性

目的分析对比门冬胰岛素与人胰岛素对妊娠合并糖代谢异常患者的有效性及安全性及其对妊娠结局的影响。方法将2004年1月1日至2010年5月31日接受孕期检查并分娩的应用门冬胰岛素控制血糖的妊娠合并糖代谢异常者纳入分析（Asp组，n=77），其中妊娠合并糖尿病（DM）患者22例、妊娠期糖尿病（GDM）患者55例。选择同期接受孕期检查并分娩的应用人胰岛素控制血糖的妊娠合并糖代谢异常患者（HI组，n=77）按1：1作为对照进行回顾性对比研究。对比2组胰岛素治疗前后血糖变化、血糖下降至正常水平所需时间、胰岛素最大用量、治疗期间低血糖事件发生率及分娩结局。2组数据比较用t检验及秩和检验。结果治疗1周后，Asp组DM患者早餐、晚餐后2h血糖分别为（6．5±1．1）和（7．1±1．1）mmol／L，HI组则分别为（8．0±1．1）和（7．8±0．8）mmol／L；而Asp组GDM患者早餐、午餐和晚餐后2h血糖分别为（6．5±0．7）、（6．8±0．7）和（6．7±0．7）mmol／L，HI组则分别为（7．1±0．9）、（7．3±0．9）和（7．4±0．8）mmol／L；Asp组餐后2h血糖水平均低于Ⅲ组，差异均有统计学意义（均P〈0．05）。Asp组DM患者早餐后2h血糖首次下降至正常水平所需时间为（3．0±2．2）d，HI组则为（5．0±2．1）d；Asp组GDM患者早餐后2h血糖首次下降至正常水平所需时间为（2．3±1．6）d，HI组则为（4．3±2．6）d；Asp组餐后血糖下降至正常水平所需时间均比HI组短，差异均有统计学意义（均P〈0．05）。Asp组低血糖事件发生率为3．9％（DM患者1例，GDM患者2例），HI组为24．7％（DM患者8例，GDM患者11例）（P〈0．05）。Asp组DM患者新生儿低血糖发生率及新生儿转儿科率分别为4．5％、36．4％，而HI组为18．2％、50．0％；Asp组GDM患者巨大儿、新生儿低血糖发生率及转儿科率分别为10．9％、3．6％、25．5％，HI组则分别为18．2％、10．9％、38．2％；Asp组的分娩结局有优于HI组的趋势，但2组间差异均无统计学意义（均P〉0．05）。结论在妊娠合并糖代谢异常孕妇中，相比人胰岛素，门冬胰岛素能更快、更有效地控制血糖，同时可明显降低低血糖事件的发生。对分娩结局的影响方面，Asp组有优于Ⅲ组的趋势。     

Fibrinolytic dysfunction after gestation is associated to components of insulin resistance and early type 2 diabetes in latino women with previous gestational diabetes

Among patients with metabolic syndrome (MS), atherosclerosis and abnormal fibrinolytic function are frequently present, mostly owing to an increase in plasminogen activator inhibitor-1(PAI-1). We analyze PAI-1 in pregnant women, both normal and with gestational diabetes (GDM) and postpartum regarding its correlation to MS surrogates. Clinical characteristics, glucose tolerance (100g-OGTT), lipids, PAI-1 antigen, insulin sensitivity (HOMA-S), and pancreatic beta-cell function (HOMA-B) were investigated in 34 women. Eleven had normal glucose tolerance (NGT) during pregnancy and 23 had GDM (all GAD antibodies-negative). All patients were studied at 28-34 weeks of gestation and 16-24 weeks after delivery (75 g-OGTT). Parameters of interest were determined using commercial test systems. During pregnancy, PAI-1 was not statistically different between NGT and GDM (47+/-25 ng/ml versus 47+/-28 ng/ml, p=0.9). After gestation, 19 (56%) women had NGT (11 of them from previous NGT group) and 15 (44%) had impaired glucose tolerance (IGT) or DM. The IGT (IGT+DM) group had higher PAI-1 (p=0.01), which did not decreased after delivery NGT-NGT before and after delivery (47+/-25 ng/ml versus 6+/-5 ng/ml; p<0.001), GDM-NGT (62+/-36 ng/ml versus 14+/-15 ng/ml; p=0.001) and GDM-IGT (39+/-20 ng/ml versus 27+/-23 ng/ml; p=0.15). PAI-1 levels were positively correlated (p<0.05) to total cholesterol (r(s)=0.37), triglycerides (r(s)=0.48), fasting plasma glucose (r(s)=0.52), 2-h plasma glucose in the OGTT (r(s)=0.58) and were negatively correlated (p<0.05) with HOMA-S (r(s)=-0.42) and HOMA-B (r(s)=-0.38). Fibrinolytic dysfunction is still present in GDM women and is associated with early development of IGT or T2DM. PAI correlated with surrogate markers of MS levels and may identify a group of women at risk for macroangiopathy.     

妊娠糖尿病孕妇骨代谢状况的研究

目的探讨妊娠糖尿病（GDM）孕妇与正常孕妇骨代谢特点的异同。方法比较67例妊娠糖尿病患者（GDM组）与13例正常糖耐量孕妇（NGT组）血钙、磷、ALP、250HD、CTx、24h尿钙、跟骨超声（SOS）等骨代谢指标的异同。然后将GDM组患者分为A、B两组,分别给予低、高两种不同剂量钙和维生素D干预至分娩前,比较两组治疗前后上述指标的差异。结果GDM组血钙、磷为（2．3±0．1）mmol／L、（1．3±0．2）mmol／L,NGT组血钙、磷分别为（2．2±0．1）mmol／L,（1．1±0．1）mmol／L（P〈0．05）;GDM组和NGT组24h尿钙均升高;GDMB组24h尿钙治疗前为（11．0±6．9）mmol／L,治疗后为（8．2±4．3）mmol／L,明显下降（P〈0．05）。结论GDM孕妇骨代谢特点和NGT孕妇基本相同,24h尿钙均显著增加。GDM可能导致血钙、磷轻度增加。补充足量的钙剂和维生素D可使尿钙丢失减少。     

2069例不同糖耐量状态孕妇的血脂谱及围生结局分析

目的在大样本群体中探讨不同糖耐量状态孕妇血脂谱及其围生结局,并寻找巨大儿发生的独立危险因素。方法50g口服葡萄糖筛查试验（GCT）1hPG≥7．8mmol／L的孕妇共2069例,按100gOGTT结果分为NGT（n=911）、IGT（n=422）和GDM（n=736）3组,并测定3组HbA1c、TG、TC、LDL-C、HDL-C水平,以上指标均在24～28孕周获得。结果（1）不同糖耐量状态的孕妇TG、TC、LDL-C、HDL-C均较非孕参考范围明显升高。从NGT—IGT—GDM组,TG逐步上升（P〈O．01）,HDL-C逐步下降（P〈0．01）,TC和LDL-C无统计学差异。（2）经过对血糖的严格干预后,3组的孕期体重增加,新生儿体重无差异,然而巨大儿的发生率在GDM和IGT组仍明显高于NGT组（14．1％,13．1％7J$6．6％,P〈0．01）。（3）二项分类Logistic回归分析发现OGTT中的FPG（OR=2．98,95％CI1．63～5．48,P〈0．01）、孕期体重增加（OR=1．12,95％CI1．06～1．19,P〈0．01）为巨大儿发生的独立危险因素,而HDL-C为独立保护因素（OR—0．41,95％C10．20～0．86,P〈0．05）。结论妊娠时,血脂各组分较非孕状态明显升高,从NGT→IGT→GDM,TG逐步上升而HDL-C逐步下降。即使经过血糖的严格干预,巨大儿的发生率并不能降低到NGT组水平。FPG水平和孕重增加是巨大儿发生的独立危险因素,而HDL-C是保护因素。     

妊娠糖尿病患者动态血糖谱的特点及其意义

目的探讨妊娠糖尿病（GDM）患者动态血糖谱的特点,为临床治疗提供依据。方法采用动态血糖监测系统（CGMS）对7例GDM患者及20名糖耐量正常者（NGT）进行连续3d的皮下组织葡萄糖监测。GDM组和NGT组平均年龄分别为28岁与41岁,体质指数分别为24、25kg／m^2。计算比较2组平均血糖水平（MBG）、血糖标准差（SDBG）、平均血糖波动幅度（MAGE）、三餐餐后血糖漂移幅度（PPGE）、日间血糖平均绝对差（MODD）及日内最大血糖波动幅度（DMMG）,并统计血糖达标后胰岛素的使用情况。组间及组内参数比较采用t检验。结果GDM组MAGE、PPGE及DMMG均较NGT者升高,分别为MAGE（4．3±0．2）比（1．6±0．3）mmol／L,早餐餐后血糖漂移幅度（BPPGE）（5．5±1．1）比（1．8±0．4）mmol／L,中餐餐后血糖漂移幅度（LPPGE）（3．1±0．3）比（1．3±0．2）mmol／L,晚餐餐后血糖漂移幅度（DPPGE）（3．4±0．4）比（1．5±0．2）mmot／L,DMMG（6．0±2．7）比（2．9±0．2）mmol／L,2组差异均有统计学意义（t=4．4、5．6、2．3、2．8、6．1,均P〈0．05）。2组MBG、SDBG、MODD差异均无统计学意义（t=0．9、1．4、0．3,均P〉0．05）。GDM患者BPPGE较LPPGE和DPPGE大,差异均有统计学意义（t=3．1、2．6,均P〈0．05）。GDM患者基础胰岛素用量占一天胰岛素总量15．0％,早餐的餐时胰岛素用量最大,占一天胰岛素总量的33．5％。结论CGMS是GDM监测血糖波动的有效手段,GDM患者以三餐后高血糖及餐后血糖波动为主,早餐血糖波动最为显著,餐时胰岛素用量为主,早餐餐时胰岛素用量最大。胰岛素用量与血糖波动的情况一致。     

中老年正常糖耐量人群胰岛β细胞功能分析

目的 分析中老年正常糖耐量人群血糖水平与胰岛B细胞分泌功能的关系.方法 选择上海市部分社区流行病学调研2095例居民,根据口服葡萄糖耐量试验(OGTT)、空腹血糖(FPG)和餐后2 h血糖(2 hPG)结果,将受检者分为正常糖耐量、糖耐量减低(IGT)、空腹血糖受损(IFG)、糖耐量减低合并空腹血糖受损(IFG/IGT)及糖尿病组.再将正常糖耐量者按年龄及空腹血糖值进行分组,观察稳态胰岛β细胞功能指数(HBCI),并对各组年龄、血糖与胰岛β细胞分泌功能指标进行统计学分析.结果 (1)随着年龄的增长,FPG逐渐升高,40～49岁、50～59岁及60～69岁组分别为(5.00±0.47)mmol/L、(5.09±0.44)mmol/L及(5.17±0.48)mmol/L,50～59岁组与40～49岁组比较(t=2.727,P<0.01)、60～69岁组与50～59岁组比较(t=2.303,P<0.05),均差异有统计学意义,但空腹胰岛素(FINS)值变化无明显规律;(2)随着年龄的增长,HBCI值呈下降趋势(F=33.75,P<0.05);(3)FPG≥5.0 mmol/L组较<5.0 mmol/L组HBCI值下降,分别为4.39±0.58和4.22±0.70,差异有统计学意义(t=2.974,P<0.05).结论 中老年正常糖耐量者随着年龄增长,空腹血糖增高;当空腹血糖≥5.0 mmol/L时,可能存在胰岛β细胞分泌功能异常.     

Maternal triglyceride levels and newborn weight in pregnant women with normal glucose tolerance.

OBJECTIVE: To determine the predictive value of serum triglyceride levels (TG) for neonatal weight in pregnant women with positive diabetic screening but normal glucose tolerance. RESEARCH DESIGN AND METHODS: We enrolled 180 pregnant Caucasian women with positive diabetic screening. All women underwent a 3-h 100-g oral glucose tolerance test (OGTT) at 27th +/- 4 week of gestation. At the time of OGTT, we measured: fasting plasma glucose, fasting lipids profile and determined ApoE polymorphisms to evaluate the effects on lipid levels. In 83 women with normal glucose tolerance and at term delivery we evaluated the association between maternal serum TG, specific maternal parameters known to affect fetal growth and newborn weight. RESULTS: Based on OGTT, gestational diabetes mellitus (GDM) was diagnosed in 36 women (20%), impaired glucose tolerance (IGT) in 23 (13%), and normal glucose tolerance (NGT) in 121 (67%). Serum TG concentration was significantly higher in women with GDM (2.47 +/- 0.77 mmol/l) as compared with NGT (1.99 +/- 0.64 mmol/l) or IGT (1.98 +/- 0.81 mmol/l) (P < 0.01). ApoE3 allelic frequency was 86%, ApoE2 and ApoE4 were 5 and 9%, respectively. We found no clear-cut association between apoE genotype and serum TG concentration. Macrosomia and LGA newborns were more frequent in IGT than in GDM or NGT (P < 0.01). In the 83 women with positive diabetic screening but normal glucose tolerance who delivered at term, the incidence of LGA infants was significantly higher in those with TG levels higher than the 75th percentile (> 2.30 mmol/l) (21%) than in mothers who had normal TG levels (4.5%) (P < 0.05). Pre-pregnancy BMI (r(2) = 0.067), weight gain during pregnancy (r(2) = 0.062), fasting serum TG (r(2) = 0.09), and 2-h post-OGTT glucose levels (r(2) = 0.044) were all associated with neonatal body weight (all P < 0.05 or less). However, on a multiple regression analysis, only pre-pregnancy BMI (F-test = 7.26, P < 0.01), and fasting serum TG (F-test = 4.07, P < 0.01) were independently associated with birth weight. CONCLUSIONS: Pre-pregnancy BMI and fasting maternal serum TG determined in the last trimester of gestation were independently associated with neonatal birth weight in women with normal glucose tolerance, but positive screening test. TG levels measured in the third trimester of pregnancy are independent of the genetic polymorphism of ApoE.     

妊娠糖尿病患者分娩后胰岛素抵抗和胰岛B细胞功能研究

目的研究妊娠糖尿病患者分娩后胰岛素抵抗、胰岛B细胞功能状态,探讨其在分娩后糖耐量异常发生发展中的作用。方法对2008-09-01—2009-07-10中国医科大学附属盛京医院内分泌科根据口服糖耐量试验筛选出8例有妊娠糖尿病史的妇女妊娠后糖耐量正常(NGT)者,另选取8例有妊娠糖尿病病史的妇女妊娠后糖耐量异常(IGT)者与之匹配。应用高胰岛素-正葡萄糖钳夹技术和静脉葡萄糖耐量试验评估胰岛素抵抗和胰岛B细胞功能。结果 NGT组和IGT组体重指数(BMI)及三酰甘油比较差异无统计学意义(P<0.05);IGT组葡萄糖输注速率(GIR)明显低于NGT组(5.70±1.14对7.79±1.75,P<0.05);NGT组胰岛素一时相分泌量高于IGT组(5.32±0.37对4.35±0.46,P<0.05);两组间胰岛素第二时相分泌量(4.35±0.31对4.38±0.56,P>0.05)比较差异无统计学意义。结论妊娠糖尿病患者分娩后糖耐量异常者较糖耐量正常者存在更为明显的胰岛素抵抗及胰岛B细胞功能缺陷。     

Relative hyperproinsulinemia as a sign of islet dysfunction in women with impaired glucose tolerance.

Proinsulin release is increased relative to insulin secretion in subjects with type 2 diabetes, indicative of islet dysfunction. However, it has not been conclusively shown whether there is an increased relative proinsulin release in subjects with impaired glucose tolerance (IGT), i.e. whether it precedes the development of diabetes. We therefore determined the proinsulin to insulin ratios in the fasting state and after acute stimulation of insulin secretion in 23 postmenopausal women, aged 61-62 yr (mean +/- SD, 61.7 +/- 0.5 yr). Ten women had normal glucose tolerance (NGT), and 13 had IGT. The groups were matched for insulin sensitivity and did not differ in body mass index. Proinsulin and insulin secretion were measured after arginine stimulation (5 g, i.v.) at three glucose levels (fasting, 14 mmol/L, and >25 mmol/L), and the acute insulin (AIR(arg)) and proinsulin responses (APIR(arg)) were calculated as the mean 2-5 min postload increase. At fasting glucose, levels of insulin, proinsulin, or the proinsulin/insulin ratio (13.6 +/- 5.0% vs. 11.1 +/- 2.7%; P = NS) did not differ between NGT and IGT. Although the AIR(arg) values were decreased in the IGT group at all glucose levels (P < 0.05), the absolute proinsulin levels and the APIRs(arg) were similar between IGT and NGT women. Therefore, the IGT women had higher proinsulin/insulin ratios at 14 mmol/L (10.7 +/- 4.4% vs. 6.4 +/- 1.8%; P = 0.006) and more than 25 mmol/L glucose (11.4 +/- 5.2% vs. 6.7 +/- 2.1%; P = 0.007). The IGT group had increased APIR(arg)/AIR(arg) at fasting (2.2 +/- 1.4% vs. 1.3 +/- 0.6%; P = 0.047) and more than 25 mmol/L glucose (3.5 +/- 1.6% vs. 2.3 +/- 0.7%; P = 0.037). We conclude that women with IGT exhibit increased relative proinsulin secretion, suggesting a defect in the intracellular proinsulin processing before diabetes develops.     

Insulin resistance has no impact on ghrelin suppression in pregnancy

Ghrelin is reduced in various states of insulin resistance. The aim of this study was to examine the relationship between ghrelin and glucose metabolism during pregnancy - a natural insulin-resistant state - in women with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or gestational diabetes mellitus (GDM) and potential changes 3 months after delivery. A total of 54 women, 37 pregnant and with various degrees of insulin resistance and 24 postpartum (PP, seven of them also studied during pregnancy) were studied. Ghrelin plasma concentrations at fasting and 60' following glucose loading (75 g-2 h-oral glucose tolerance test), area under the curve of plasma glucose (G-AUC(OGTT)) and insulin sensitivity [homeostatic model assessment (HOMA) and oral glucose sensitivity index (OGIS) indices, respectively] were determined. Both baseline and 60' ghrelin concentrations were to a comparable degree ( approximately by 65%) suppressed in NGT, IGT and GDM as compared to the PP group (the latter being indistinguishable from NGT regarding glucose tolerance and insulin sensitivity). In all women studied both during and after pregnancy, ghrelin levels rose from pregnancy to PP (mean increase 313.8%; P < 0.03). There was no correlation between baseline ghrelin and insulin sensitivity as estimated from both baseline (HOMA) and dynamic (OGTT:OGIS) glucose and insulin data. Ghrelin is substantially decreased during pregnancy, but glucose-induced ghrelin suppression is preserved at a lower level. There is apparently no relation to the degree of insulin resistance.