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。     

纳格列奈-口服葡萄糖耐量试验对检测正常人胰岛β细胞功能的评价

目的 优化纳格列奈-口服葡萄糖耐量试验(NG-OGTT)评估胰岛β细胞功能的方法.方法 对24例健康志愿者进行NG-OGTT,测定各设定时间点(-15、0、10、20、30、45、60及120 min)的胰岛素和血糖水平.胰岛素测定采用放射免疫法.观察NG-OGTT中胰岛素释放的峰值,胰岛素释放倍增值(MVI),各设定时间点的胰岛素释放曲线下面积(AUCIns)、胰岛素释放速率(IRV)、胰岛素净增值与血糖净增值的比值(△I/△G),筛选出NG-OGTT中最能反映胰岛β细胞分泌与储备功能的时间点.结果 (1) 正常人在NG-OGTT中反映胰岛β细胞早期相分泌功能的胰岛素释放峰值(90.50 mU/L)与IRV(2.75 mU·L-1·min-1)的达峰时间均在糖负荷后30 min;(2)其△I/△G的达峰时间虽在糖负荷后45 min(56 mU/mmol),但45 min时该值的升高主要由血糖的快速降低引起;(3) 反映β细胞储备功能的MVI(18.8)的达峰时间亦在糖负荷后30 min;(4) 其AUCIns在60 min时与120 min具有显著性相关(r=0.901,P=0.000).结论 糖负荷后采用-15、0、30和60 min 4个采血点,能反映β细胞早期相分泌功能及储备功能,方法简便.     

那格列奈-OGTT测定LADA患者及其一级亲属的胰岛β细胞功能

目的　以那格列奈 (NG) 口服葡萄糖耐量试验 (OGTT)方法评估LADA患者及其一级亲属(FDR)胰岛 β细胞功能。 方法　 9例正常人 1周内先后行NG OGTT、精氨酸刺激试验和普通OGTT ,测定各时点的胰岛素和血糖水平。观察NG OGTT中胰岛素净增值与血糖净增值的比值 (ΔI/ΔG)和精氨酸刺激试验中急性期胰岛素释放 (AIR)的相关性 ,比较NG OGTT和普通OGTT的差异和关联。 10例FDR行NG OGTT和普通OGTT ,LADA和 2型糖尿病 (DM)患者各 9例仅行NG OGTT ,比较 4组研究对象在NG OGTT中的早期相胰岛素释放和胰岛 β细胞储备功能 ,并用HOMA公式评估胰岛素抵抗。 结果　 (1)NG OGTT中胰岛素释放速率 (IRR)最高点为糖负荷后 3 0min ,且该时点的ΔI3 0 /ΔG3 0 与精氨酸刺激试验的AIR呈正相关 (Rs =0 .674,P <0 .0 5 ) ;NG OGTT中各时点胰岛素曲线下面积和胰岛素释放倍增值均高于普通OGTT(均P <0 .0 1)。 (2 )LADAFDR在NG OGTT中ΔI3 0 /ΔG3 0 (2 3 .0± 13 .2 )mU/mmol和 3 0min处IRR (1.3± 0 .8)mU·L-1·min-1均低于正常 (P <0 .0 5 ) ,而HOMA IR指数高于正常 (2 .2± 0 .7vs 1.5± 0 .7,P <0 .0 5 )。 (3 )LADA和 2型DM患者的HOMA IR指数分别为 (2 .9± 0 .9和 5 .0± 3 .4) ,均高于正常 (1.5± 0 .7) (2型DM >LADA >正常     

成人单纯性肥胖患者的胰岛β细胞功能探讨

为探讨成人单纯性肥胖患者的胰岛β细胞功能,我们对52例患者和30例正常健康人进行了口服葡萄糖耐量试验(OGTT)及胰岛素释放(OGIRT)检测。现报告如下。1.一般资料:正常对照组30例,均为健康人。单纯肥胖组52例,体重均超过标准体重的20%,体重指数为24%～36%。2.检查方法及结果:受试者前3天进正常饮食,试验前12小时禁食,次晨空腹釆血,口服葡萄糖100g(溶于300～400ml水     

肺源性心脏病患者胰岛功能与糖代谢异常分析

目的了解肺源性心脏病胰岛功能状态,分析肺源性心脏病糖代谢异常的原因.方法选择无糖尿病的肺源性心脏病急性加重期患者36例,进行胰岛素释放试验,并同健康对照组相对照.分析糖耐量及胰岛素释放曲线特征.结果同健康对照组比较,肺源性心脏病患者血糖峰值为(8.46±0.61)mmol/L,显著高于对照组(7.59±0.50)mmol/L(P＜0.01),峰值时间缩短;肺源性心脏病患者,胰岛素峰值为(47.2±21.1)μu@mL,显著低于对照组(77.1±38.2)μu@mL-1(P＜0.01),胰岛素峰值时间延长,曲线平坦.结论肺心病患者糖代谢异常,可能与胰岛素分泌不足和胰岛素灭活障碍有关.     

以(FINS×FPG)/(PG2h+PG1h-2FPG)评估胰岛β细胞分泌功能的可行性探讨

目的　探讨以一个修正的 β细胞胰岛素分泌指数 (MBCI) =(FINS×FPG) / (PG2h PG1h- 2FPG) (FINS :空腹胰岛素 ;FPG :空腹血浆血糖 ;PG2h、PG1h :口服葡萄糖耐量试验 2h、1h血浆血糖 )评估 β细胞胰岛素分泌功能的可能性。方法　在 430例糖耐量正常 (NGT)和糖耐量低减 (IGT)人群中分析 (FINS×FPG) / (FG2h PG1h - 2FPG)分辨血糖水平不同组间 β细胞功能差别的能力 ,并与应用胰岛素增值与血糖增值比值 (ΔI/ΔG)及HOMA胰岛素分泌指数 (HBCI) =2 0×FINS/ (FPG - 3 5 )的结果比较。结果　偏相关分析显示 ,在调整胰岛素敏感性影响后 ,在NGT人群HBCI与PG1h仅边缘相关(P =0 0 5 8) ,ΔI/ΔG与PG2h相关不显著 (P =0 2 3) ,而MBCI与PG1h、PG2h均显著相关 (P =0 0 0 0 1)。在含IGT与NGT的总组 ,MBCI比HBCI及ΔI/ΔG与PG1h及PG2h相关更密切 (与PG1h相关系数分别为 - 0 787,- 0 5 34及 - 0 5 0 7;与PG2h相关系数分别为 - 0 76 6 ,- 0 5 13及 - 0 396 )。MBCI及HBCI还能区别某些PG2h仅相差 1 10mmol/L的IGT亚组间 β细胞功能差别 ,ΔI/ΔG未能做出这种分辨。结论　 (FINS×FPG) / (FG2h PG1h - 2FPG)与HBCI和ΔI/ΔG都能分辨NGT和IGT组的 β细胞功能差别 ,但前一指数比后两个与糖负荷后血糖水平相关更     

增龄对大鼠胰岛β细胞功能的影响

目的观察不同月龄大鼠的糖代谢指标变化,了解在基础和糖刺激下增龄对大鼠胰岛β细胞功能的影响。方法以4月龄（青年组,n=15）、14月龄（中年组,n=15）和24月龄（老年组,n=15）健康雄性Wistar大鼠为研究对象,进行口服葡萄糖耐量试验（OGTT）和胰岛素释放试验（IRT）,比较三组间基础血糖和胰岛素水平的差异,计算糖负荷后胰岛素增值与血糖增值的比值（ΔI10/ΔG10）,120min葡萄糖、胰岛素曲线下面积（AUCg,AUCi）,葡萄糖与胰岛素曲线下面积比值（AUCi/g）,胰岛素抵抗指数（HOMA-IR）,胰岛β细胞功能指数（HOMA-β）等,以分析各组间胰岛功能的差异。结果随着月龄的增长,空腹血糖有升高的趋势,但未达到统计学差异。OGTT后老年组大鼠表现为血糖达峰时间延长,血糖峰值增加,OGTT2h血糖及AUCg增加,即老年组大鼠出现糖耐量异常状态,主要表现为餐后高血糖。青年组、中年组和老年组大鼠空腹胰岛素水平分别为（0.59±0.14）、（1.60±0.15）、（2.37±0.04）μg/L（两两相比均P〈0.01）;IRT中,老年组大鼠胰岛素达峰时间延迟,ΔI10/ΔG10降低,AUCi增加（P〈0.05）。使用稳态模型评估,HOMA-β在青年、中年和老年组中呈递增趋势,但未达到统计学差异;而HOMA-IR在青年、中年和老年组分别为3.09±0.80、8.34±0.72、13.14±1.59（两两相比均P〈0.01）。结论正常老龄大鼠存在一定的胰岛素抵抗和代偿性胰岛素分泌增加,但由于胰岛素分泌的早期时相受损,仍然出现糖负荷后血糖增高状态。     

一种检查LADA一级亲属β细胞功能的新方法--那格列奈-OGTT试验临床应用评价

研究目的:(1)对那格列奈(NG)口服葡萄糖耐量试验(OGTT)评价胰岛β细胞功能的方法予以优化;(2)应用NG OGTT综合评价成人隐匿性自身免疫性糖尿病(LADA)和2型糖尿病(DM)患者一级亲属的胰岛β细胞功能及胰岛素抵抗(IR)状况[1,2]。方法:(1)对24例健康对照行NG OGTT。观察NG NGTT中胰岛素释放的峰值,胰岛素释放倍增值(MVI),各设定时间点的胰岛素释放曲线下面积(AUCIns)、胰岛素释放速率(IRR)、ΔI/ΔG,筛选出NG OGTT中最能反映胰岛β细胞分泌功能的时间点。(2)对39例谷氨酸脱羧酶抗体(GADA)阳性LADA患者的一级亲属〔血糖…     

应用INGAP多肽体外分步诱导胰岛新生研究

目的 应用INGAP多肽在体外建立新的分步诱导分化体系诱导胰岛新生. 方法 分离纯化SD大鼠的胰腺导管干细胞.并体外扩增培养,取2～6代细胞进行分步诱导分化,于分化末期添加INGAP多肽,待诱导结束后收获新生类胰岛样细胞团(ILCs)分别行免疫荧光和RT-PCR检测,并通过葡萄糖刺激的胰岛素释放试验(GSIS)评价ILCs的胰岛素分泌能力. 结果 (1)分离纯化的胰腺导管干细胞经过四步诱导后最终可形成立体结构的ILCs,其insulin和glucagon染色均为阳性,RT-PCR检测该ILCs也有insulin和glucagon基因的表达.(2)GSIS结果:新生ILCs和新分离胰岛的高糖组胰岛素释放量均显著高于低糖组(P＜0.01);新生ILCs的胰岛素刺激指数接近新分离胰岛(P＞0.01). 结论 通过建立新的包含INGAP多肽的体外分步诱导分化体系,能够获得具有立体结构和一定胰岛素分泌能力的立体ILCs,为获取胰岛移植所需的β细胞提供了更有效的方法.     

营养和代谢疾病

642492 胰岛素释放试验在糖尿病分型中的探讨超楚生等湖南医学2(2):10～14,1985 对28例糖尿病人作口服葡萄糖耐量试验和胰岛素释放试验,与30名正常人作对照。结果正常人口服75g萄葡糖的耐糖量试验正常。非胰岛素依赖型糖尿病大多数患者胰岛素释放延迟,服糖后30分钟和1小时胰岛素释放指数明显低于正常人,3小时则     

空腹血糖水平与精氨酸刺激后胰岛素急性分泌的关系

目的 探讨不同糖代谢状况下空腹血糖水平与精氨酸刺激后胰岛素急性分泌的关系.方法 入选2004至2005年来我院门诊就诊者及健康志愿者626例,其中糖耐量正常114例,糖耐量受损60例,新诊断2型糖尿病452例.在我院内分泌科门诊接受葡萄糖耐量试验及精氨酸试验.测定空腹血糖、胰岛素原及真胰岛素水平,评估精氨酸刺激后胰岛素急性分泌相(△TI).采用稳态模型计算胰岛素抵抗指数(HOMA-IR).运用协方差分析或非参数检验进行统计学分析.结果 空腹血糖为3.8～5.0 mmol/L时,△TI由34.13 mmol/L逐渐升至41.50 mmol/L;空腹血糖为5.0 mmol/L时,△TI达到峰值41.50 mmol/L,之后轻度下降;空腹血糖为6.1～10.0 mmol/L时,△TI持续下降并形成平台,较峰值降低近35%;空腹血糖>10.0 mmol/L时,△TI显著减退;空腹血糖>11.1 mmol/L时,△TI达17.40 mmol/L,较峰值降低近60%.空腹血糖为3.8～6.1 mmol/L时,胰岛素原分泌迅速由0.01 pmol/L增至6.96 pmol/L;空腹血糖为6.1～10.0 mmol/L时,胰岛素原分泌持续缓慢增加,并达到峰值10.84 pmol/L;空腹血糖>10.0 mmol/L时,胰岛素原分泌呈显著下降趋势.空腹血糖由3.8 mmoL/L增至7.8 mmol/L时,HOMA-IR呈上升趋势;空腹血糖>7.8 mmol/L时,HOMA-IR维持较高水平(6.82)并处于平台.结论 空腹血糖为6.1～10.0 mmol/L时,精氨酸刺激后胰岛素急性分泌相相对稳定,表明胰岛β细胞尚具有较好的储备功能.空腹血糖>10.0 mmol/L时,精氨酸试验激发后△TI及胰岛素原显著下降,提示胰岛β细胞功能严重衰竭.     

糖尿病前期患者肾小球滤过率影响因素的相关分析

目的 探讨影响糖尿病前期患者肾小球滤过率(GFR)的危险因素.方法 自2007年1月至2009年7月,对南通大学第二附属医院内分泌科门诊通过75g口服葡萄糖耐量试验筛查出的糖尿病前期患者165例,按1999年世界卫生组织诊断标准,分为空腹血糖受损组(IFG组,42例)、糖耐量减低组(IGT组,56例)、IFG合并IGT组(CGI组,64例),并选取同期体检正常的人群作为对照组(NGT组,30例).检测各组空腹血糖、胰岛素、糖负荷后2h血糖(Gluc120),GFR等,计算稳态时各组胰岛素抵抗指数(HOMA-IR)、胰岛细胞分泌功能指数(HOMA-B%)和糖负荷状态下早相胰岛素分泌指数(ΔI30/ΔG30)、第二时相胰岛素分泌指数(AUC120).统计学采用Pearson线性相关分析及多元线性逐步回归分析.结果 (1)GFR在NGT、IFG、IGT、CGI组依次升高,组间比较差异具有统计学意义[各组GFR分别为(103±12、113±13、133±16、143±14)ml/min,P<0.05];(2)线性相关分析示GFR与体重指数、HOMA-IR、空腹胰岛素、Gluc120、AUC120呈正相关(r值分别为0.571、0.842、0.606、0.788、0.528,均P<0.01),GFR与ΔI30/ΔG30呈负相关(r=-0.628,P<0.01);(3)逐步回归分析示GFR的影响因素是HOMA-IR、Gluc120、ΔI30/ΔG30、AUC120(β值分别为0.631、0.343、-0.198、0.248,均P<0.05).结论 初步考虑糖尿病前期患者GFR增高的危险因素是HOMA-IR、Gluc120、AUC120升高和ΔI30/ΔG30降低,早期干预糖尿病肾病的发生发展需要控制血糖、减轻胰岛素抵抗和改善胰岛细胞功能.     

Clustering of impaired glucose tolerance, hyperinsulinemia and dyslipidemia in young north Indian patients with coronary heart disease: a preliminary case-control study

Metabolic insulin resistance syndrome is a critical factor in the pathogenesis of atherosclerosis and coronary heart disease in Indians. In a preliminary case-control study, 44 young patients (age < 40 years) with coronary heart disease (angina, myocardial infarction), not previously diagnosed to have diabetes mellitus, were recruited seven days to six weeks after the cardiac event (group I), and compared to 20 healthy subjects (group II). After recording history and anthropometric data, they were subjected to oral glucose tolerance test. Each group was divided into A and B subgroups according to the magnitude of impaired glucose tolerance. Hypertension was recorded in 11 (25%) patients in group I, while all the subjects in group II were normotensive (p < 0.05). Groups IB and IIB, consisting of subjects with impaired glucose tolerance displayed significantly high post-load blood glucose values. After excluding patients with the family history of diabetes mellitus, there were 13 (39%) and 3 (17%) patients with impaired glucose tolerance in groups I and II, respectively. Total cholesterol and low-density lipoprotein cholesterol levels were higher in group I as compared to group II (p < 0.01). Group IB showed highest mean values of total cholesterol, triglycerides, low-density lipoprotein cholesterol and lowest level of high-density lipoprotein cholesterol as compared to other subgroups. Serum insulin levels at 30 and 90 minutes were significantly higher in group I (p < 0.05). Group IB and IIB showed higher insulin values at 90 minutes when compared to group IA (p < 0.05) and IIA (p < 0.05). Elevated serum insulin values at 90 minutes during oral glucose tolerance test could differentiate among both groups and subgroups, except IB versus IIB. The study demonstrates significantly high prevalence of hypertension, obesity, impaired glucose tolerance, hyperinsulinemia and dyslipidemia, suggesting fully developed metabolic insulin resistance syndrome in young north Indian patients with manifest coronary heart disease.     

Serum high-molecular weight adiponectin decreases abruptly after an oral glucose load in subjects with normal glucose tolerance or impaired fasting glucose, but not those with impaired glucose tolerance or diabetes mellitus

Adiponectin exists in the blood as 3 forms, which are a trimer, a hexamer, and a high-molecular weight (HMW) form. We investigated whether circulating HMW adiponectin levels were altered by oral glucose or fat ingestion. Forty male subjects underwent a 75-g oral glucose loading test (OGTT), and 11 healthy subjects (5 women and 6 men) received a fat loading test. Serum levels of HMW and total adiponectin were measured during the OGTT and the fat loading test. The fat loading test was performed for at least 8 hours. Among the 40 male subjects, 11 had normal glucose tolerance (NGT), 9 had impaired fasting glucose (IFG), 11 had impaired glucose tolerance, and 9 had diabetes mellitus (DM). In all 40 subjects, the serum total adiponectin level did not change significantly, whereas serum HMW adiponectin decreased significantly after a glucose load and reached 92.2% of the basal level at 120 minutes after the OGTT (P < .01). The HMW to total adiponectin ratio decreased significantly from 0.47 ± 0.15 at baseline to 0.43 ± 0.13 at 120 minutes after a glucose load (P < .05). Serum HMW adiponectin measured at 120 minutes after the OGTT decreased significantly to 86.0% and 85.6% of the basal level in subjects with NGT or IFG, respectively (both P < .01). In subjects with impaired glucose tolerance or DM, however, serum HMW adiponectin did not change. The area under the curve for insulin at 30 minutes after a glucose load during the OGTT was significantly larger in subjects with NGT or IFG than in those with DM (P < .05). In addition, the insulinogenic index (ΔI_0-30/ΔG_0-30) was significantly higher in subjects with NGT or IFG than in those with DM (P < .001). Percentage changes in serum HMW adiponectin of the baseline at 120 minutes correlated negatively with those in serum insulin (r = −0.468, P = .0023), but not plasma glucose, of the baseline at 30 minutes in 40 subjects. On the other hand, serum triglycerides increased significantly after an oral fat load in 11 healthy subjects; but neither serum total nor HMW adiponectin changed. In conclusion, serum HMW adiponectin (but not total adiponectin) decreased rapidly after glucose loading in subjects with NGT or IFG; and the decrease of HMW adiponectin may be associated with an increase of serum insulin at 30 minutes.     

Characteristics of Japanese subjects who progress from normal to impaired glucose tolerance. Longitudinal study excluding changes in body weight

In this retrospective longitudinal study, we focused on the clinical characteristics of Japanese individuals with recent onset impaired glucose tolerance (IGT) who have been followed up for insulin secretory function and 75-gram oral glucose tolerance test (OGTT) for more than 3 years annually before they progressed from normal glucose tolerance (NGT) to IGT. Subjects whose body weight did not show significant change for the period were selected and labeled as either NGT (no change in OGTT over 3 years) or IGT (progressors from NGT to IGT) groups (n = 24, each). We compared the basal biochemical data and response of plasma glucose and serum insulin after OGTT of the two groups. In the IGT progressors, significant increase of plasma glucose at 30 to 120 minutes during OGTT and significant decrease of HDL-cholesterol were observed since 3 years before onset of IGT. In addition to increase of serum glucose and decrease of HDL-cholesterol, serum insulin at 120 minutes during OGTT were significantly and remarkably high at onset and 3 years before onset of IGT. Plasma glucose at 30-120 minutes and serum insulin level at 120 minutes after glucose load are potentially significant predictors of progression from NGT to IGT even in subjects who do not show increase of body weight.     

Glucose metabolism in children with renal failure: oral or intravenous glucose tolerance.

There is debate about the most suitable test for investigation of glucose tolerance in children with chronic renal failure. We therefore studied the agreement between the two most commonly used glucose tolerance tests in 33 children with chronic renal failure (mean age 10.9+/-5.3 years, median GFR was 24 ml/min/1.73 m2). All children underwent an oral glucose tolerance test (OGTT) with blood sampling up to 180 minutes and after an oral load of 1.75 g/kg and a standard intravenous glucose tolerance test (IVGTT) using 0.5 g/kg i.v. The two tests were performed at an interval of 23+/-5 days, with 9 patients having the OGTT before and 24 after the IVGTT. In order to account for the differing glucose load, a subgroup of 19 patients also received a glucose infusion test (GIT) using a total of 1.75 g/kg i.v. On IVGTT, 27 patients had a normal and 6 had a pathological glucose decay constant (k-value). On OGTT, 12 patients had an impaired glucose tolerance (IGT) and 3 patients were diabetic according to WHO standard, and only 18 patients had a normal glucose tolerance. While there was good correlation between both glucose and insulin concentrations between IVGTT and OGTT, only when reapplying the WHO criteria of a glucose concentration below 6.7 mmol/l to the concentration measured 180 minutes instead of 120 minutes after oral glucose load, the agreement between the two tests improved. The proportion of normal findings on GIT when compared to OGTT was identical. When using the appropriate definitions for normal and abnormal carbohydrate tolerance, interestingly the insulin (IRI) concentrations on OGTT were not discriminative between the normal and the pathological group, whereas IRI first phase secretion on IVGTT and IRI 0-180 AUC on GIT did discriminate. We conclude that the standard WHO OGTT criteria may have to be reconsidered in children with chronic renal failure and that OGTT should be extended to 180 minutes. The IVGTT, particularly when insulin early phase secretion (at 0, 1, 3 and 5 minutes) is also monitored, provides a reliable test for assessing glucose tolerance in children with chronic renal failure.     

正常糖调节人群早期相胰岛素分泌与血糖波动的关系

目的 探讨正常糖调节者早期相胰岛素分泌与血糖波动水平的关系.方法 应用动态血糖监测系统对全国10个中心339名正常体质量、正常糖调节者[年龄20～69岁,男169名,女170名,体重指数(22.2±2.2)kg/m2]进行动态血糖监测(CGM)、75 g 口服葡萄糖耐量试验及胰岛素释放试验,采用CGM监测结果计算得到的平均血糖波动幅度(MAGE)评估血糖波动,以△I30/△G30评估糖负荷后早期相胰岛素分泌,以稳态模式分析法(HOMA)评价基础胰岛素抵抗(HOMA-IR)和胰岛β细胞分泌功能(HOMA-β),以Cederhom公式计算的胰岛素敏感性指数(ISIc)评估糖负荷后胰岛素敏感性.结果 (1)339名正常人MAGE水平为(1.92±0.89)mmol/L,根据MAGE四分位间距将正常人分为四组,分别是A组83名(MAGE<1.33 mmol/L)、B组85名(MAGE 1.33～1.72 mmol/L)、C组86名(MAGE 1.73～2.41 mmol/L)及D组85名(MAGE>2.41 mmol/L).校正年龄、性别及HOMA-IR后,A、B组△I30/△G30水平高于C、D组(P<0.05或0.01),而四组间HOMA-β的差异均无统计学意义(P>0.05).(2)胰岛素敏感性方面,无论是HOMA-IR还是ISIc,四组之间的差异均无统计学意义(P>0.05).(3)Spearman相关分析显示:MAGE水平与年龄呈正相关(r=0.157,P=0.004),与△I30/△G30呈负相关(r=-0.270,P<0.001).逐步多元回归分析显示:△I30/△G30与MAGE水平呈独立负相关(β=-0.246,P<0.001).结论 正常糖调节者血糖波动水平与早期相胰岛素分泌功能密切相关.     

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。     

不同糖耐量人群血清25(OH)D3水平及与胰岛β细胞功能的关系

目的 比较不同糖耐量人群血清25(OH)D3水平,分析其与胰岛β细胞功能的关系.方法 共纳入131例受试者,包括新诊断2型糖尿病患者(T2DM组)50例,糖调节受损者(IGR组)45名和糖耐量正常者(NGT组)36名.收集临床资料并检测相关生化指标,采用酶联免疫吸附法测定空腹血清25(OH)D3水平.结果 NGT组、IGR组和T2DM组血清25(OH)D3水平依次下降(F=25.984,P＜0.05).血清25 (OH)D3与体重指数、腰围、臀围、腰臀比、空腹血糖、口服葡萄糖耐量试验2 h血糖(2 hPG)呈负相关(r=-0.600 ～-0.175,P均＜0.05),与空腹胰岛素(FINS)、胰岛素曲线下面积、稳态模型评估-胰岛β细胞功能指数、早相胰岛素分泌指数(△INS30/△G30)呈直线正相关(r=0.296～0.693,P均＜0.05).多元逐步回归分析显示,2hPG、△INS30/△G30是血清25(OH)D3水平的独立相关因素(β=0.204,-0.178,P均＜0.05).结论 IGR者与T2DM患者25(OH)D3水平降低.血清25(OH)D3与胰岛素分泌功能呈正相关,与肥胖、血糖水平呈负相关.     

Insulin sensitivity, glucose effectiveness, and insulin secretion in nondiabetic offspring of patients with non-insulin-dependent diabetes mellitus: a cross-sectional study.

To evaluate the factors that determine the worsening of intravenous glucose tolerance in subjects at high risk for developing non-insulin-dependent diabetes mellitus (NIDDM), 15 glucose-tolerant offspring of NIDDM patients and 21 control subjects were studied. Each subject underwent a frequently sampled intravenous glucose tolerance (FSIGT) test. The intravenous glucose tolerance index (K(G) index) was calculated between minutes 10 and 40 of a FSIGT test. Insulin sensitivity (S(I)), glucose effectiveness at zero insulin (GEZI), and first- and second-phase insulin responsiveness (phi1 and phi2) were estimated using glucose and insulin kinetic minimal models. The acute insulin response to glucose (AIRg) was calculated as the area under the insulin curve above the basal level between 0 and 10 minutes, and the suprabasal insulin effect was determined by the product of S(I) times AIRg. Offspring had a lower S(I) than control subjects (14.1 +/- 7.5 v 9.25 +/- 4.20 x 10(-5) x min(-1)(pmol x L(-1))(-1), P < .01), and their AIRg was similar (3,284 +/- 2,280 v 3,105 +/- 1,499 pmol x L(-1), NS). Sample division according to the median K(G) value showed that control subjects with low tolerance had a lower AIRg (4,417 +/- 2,531 v 2,043 +/- 1,068 pmol x L(-1), P < .05) and a lower suprabasal insulin effect (0.057 +/- 0.03 v 0.023 +/- 0.009 min(-1), P < .05) than control subjects with high tolerance. Offspring with low tolerance had a lower AIRg (2,574 +/- 1,197 v 3,707 +/- 1,656 pmol x L(-1), P < .05) and a lower GEZI (0.101 +/- 0.05 v 0.212 +/- 0.08 x 10(-1) x min(-1), P < .05) than offspring with high tolerance. Offspring with high and low tolerance showed lower phi1 (375 +/- 155 v 272 +/- 181 v 698 +/- 336 (pmol x L(-1))min(mmol x L(-1)), NS) than control subjects with high tolerance. In conclusion, our data suggest that decreases in GEZI and AIRg are the main factors responsible for the worsening of intravenous glucose tolerance in the offspring of NIDDM patients.