血清C-肽筛查成人自体免疫糖尿病及其临床意义

早期发现成人自体免疫糖尿病 (LADA)并及早应用胰岛素治疗是保护胰岛 β细胞功能的关键。 39例LADA和 39例 2型糖尿病 (T2DM )患者在年龄 ,性别 ,糖尿病病期等方面互相匹配。谷氨酸脱羧酶 (GAD)抗体 (Ab)阳性者确诊LADA。LADA组的平均C 肽水平为 (1 0± 0 2 )ng/ml,T2DM组为 (5 1± 0 4 )ng/ml。LADA组仅仅 1例C 肽 >正常 ,而T2DM组全部病例C 肽正常或 >正常。成人期起病的糖尿病患者 ,凡C 肽水平升高者 ,可以排除LADA。筛查中随意C 肽水平低于正常或者正常 ,应该测定GAD Ab ,阳性者确诊LADA。LADA确定诊断时的年…     

GAD65反应性T细胞检测在成人隐匿性自身免疫糖尿病筛查中的应用研究

目的探讨酶联免疫斑点试验(ELISPOT)检测谷氨酸脱羧酶反应性分泌IFN-γT细胞(GAD65-T)在成人隐匿性自身免疫糖尿病(LADA)筛查中的应用。方法选择2014年至2016年福建医科大学附属泉州第一医院收治的LADA患者28例,2型糖尿病(T2DM)40例,健康对照20例,放射配体法检测GAD65-Ab,连续密度梯度离心法分离人外周血单个核细胞(PBMC),ELISPOT法检测GAD65-T细胞。将40例T2DM分为GAD65-T细胞ELISPOT检测阳性及阴性组,比较两组的临床特征。结果 GAD65-T细胞数(中位数及95%CI)LADA组为7.2(1.9~11.1)个,T2DM组为3.6(2.9~6.0)个,对照组为0.9(0.2~1.7)个。LADA组的细胞数明显高于T2DM及对照组(P均0.01);T2DM较对照组具有更高频率的细胞数(P0.05)。以大于95%CI(对照组)判为阳性,LADA,T2DM及对照组的阳性率分别为71.4%(20/28)、32.5%(13/40)、0。40例T2DM亚组分析显示GAD65-T细胞ELISPOT检测阳性组较阴性组的患者BMI更低、血糖控制更差、空腹C肽水平更低。结论部分GAD65-Ab阴性的T2DM患者存在GAD65-T细胞,联合GAD65-T细胞ELISPOT及GAD65-Ab检测可明显提高LADA的检出率。     

两种成人隐匿性自身免疫糖尿病亚型的谷氨酸脱羧酶抗体界值的探讨

目的　探讨判别两种成人隐匿性自身免疫糖尿病(LADA)亚型的最佳谷氨酸脱羧酶抗体(GAD-Ab)界值及其诊断价值。　方法　绘制LADA患者GAD-Ab指数的频数分布图,进行曲线拟合。比较130例经典1型糖尿病、145例2型糖尿病和145例LADA患者的临床特点,利用受试者运筹特征(ROC)曲线比较不同GAD-Ab滴度对LADA患者中反映 LADA 1 型特征的胰岛素缺乏和反映LADA 2型特征的代谢综合征(MS)的诊断价值,确定诊断两种 LADA亚型的最佳 GAD-Ab界值。用放射配体法测定 GAD-Ab。　结果　(1) GAD-Ab 频数在 LADA患者中呈双峰分布模式。(2)以GAD Ab指数0.3为切点所区分的两组LADA患者具有差异的临床特征最多。(3)ROC曲线显示GAD Ab指数0.3是区分两种LADA亚型的最佳界值,其对胰岛素缺乏和MS诊断的敏感性和特异性分别为54 5%和92 1%,ROC曲线下面积为 0.79(与 0.5 相比,P<0.01)。　结论　GAD Ab指数0 3是区分LADA-1型和LADA-2型的最佳界值。     

LADA患者血清胰岛素原水平及其意义

目的 探讨成人隐匿性自身免疫性糖尿病(LADA)患者血清胰岛素原(PI)的分泌特征及其意义.方法 36例LADA患者、37例2型糖尿病患者和43名正常对照者均行口服糖耐量试验(OGTT),检测空腹和2 h血糖、胰岛素原(FPI和PPI)和C肽(FCP和PCP)水平,放射配体法测定谷氨酸脱羧酶抗体(GAD-Ab).结果 (1)LADA组FPI和PPI均低于2型糖尿病组(均P<0.05),但均较对照组升高(P<0.05或P<0.01);FPI/FCP和PPI/PCP(%)较2型糖尿病和正常对照均增高(P<0.05或P<0.01);(2)LADA-1型(GAD-Ab≥0.3)的PI低于LADA-2型(0.05≤GAD-Ab<0.3)(P<0.05或P<0.01),而PI/C肽均高于LADA-2型(均P<0.05);而LADA-2型与2型糖尿病差异无统计学意义;(3)LADA患者的GAD-Ab滴度与FPI和PPI呈显著负相关(r为-0.236和-0.268,均P<0.05),与PPI/PCP呈显著正相关(r=0.254,P=0.030);(4)FPI/FCP"不成比例"增高者占LADA、2型糖尿病和正常组的百分比分别为77.8%、62.2%和2.3%,PPI/PCP增高者为83.3%、51.4%和2.3%.结论 LADA患者和2型糖尿病患者一样,亦存在高PI血症,且"不成比例"PI异常增多在LADA更为显著,可能与免疫凶素有关.     

成人隐匿性自身免疫性糖尿病的临床特征分析

目的:探讨成人隐匿性自身免疫性糖尿病(LADA)的临床特征.方法:选取我院收治的LADA患者、1型糖尿病(T1DM)患者、2型糖尿病(T2DM)患者研究对象.比较三组人群一般情况、胰岛素抵抗、胰岛β-细胞功能情况、LADA与T1DM抗体分布情况、三组人群并发症.结果:T1DM组患者的年龄、体质量指数小于其他两组患者,而...     

维生素D对LADA患者胰岛β细胞功能的影响

为探讨维生素D对成人隐匿性自身免疫性糖尿病(LADA)患者胰岛β细胞功能的影响,本研究对临床初诊为2型糖尿病(DM)的患者进行谷氨酸脱羧酶抗体(GAD Ab)检测,筛选出GAD Ab阳性的LADA患者。纳入病程≤5年和空腹C肽≥0.2nmol/L的LADA患者62例,首先对患者的GAD Ab滴度和空腹C肽水平进     

LADA患者胰岛β细胞功能的前瞻性研究

目的　探讨成人隐匿性自身免疫糖尿病 (LADA)患者胰岛功能变化的特点及其影响因素。方法　 2型糖尿病 (DM )中谷氨酸脱羧酶抗体 (GAD Ab)阳性的LADA患者 16例和GAD Ab阴性的 2型DM患者 2 4例 ,分别于第 0、6、12、3 0、3 6、42和 48个月进行随访 ,测定空腹C肽 (FCP)和 10 0 g馒头餐后 2hC肽 ( 2hCP)及糖代谢指标。采用放免法测定GAD Ab和C肽。结果　LADA组的FCP于第 3 0、3 6、42、48个月明显下降 ,而C肽较入组时下降 5 0 %以上者所占百分比则均于第 12个月时明显增加 (P <0 .0 5 ) ,2型DM组的胰岛功能在随访期间则无显著性变化。LADA入组时的GAD Ab滴度与随访结束时FCP下降的差值 (ΔFCP)呈正相关 (rs=0 .5 0 ,P =0 .0 5 ) ,而体重指数 (rs=-0 .64 ,P <0 .0 1)、发病年龄 (rs=-0 .5 7,P <0 .0 5 )与ΔFCP呈负相关 ,空腹血糖 (rs=0 .64 ,P <0 .0 1)与ΔFCP呈正相关。经多元逐步回归分析 ,GAD Ab、性别、发病年龄和病程为LADA患者胰岛 β细胞功能的影响因子。 结论　LADA患者胰岛 β细胞功能较 2型DM下降更快 ,GAD Ab滴度是预测胰岛功能减退速度的重要因素 ,而且发病年龄轻、男性和病程较长对LADA患者的胰岛 β细胞功能的减退亦有一定预测作用。     

左旋精氨酸刺激试验评价遗传背景对正常糖耐量者和初诊糖尿病患者胰岛β细胞功能的影响

目的 探讨遗传背景对左旋精氨酸(L-ARG)刺激后胰岛β细胞第一时相分泌功能的影响.方法 检测201例L-ARG刺激前后胰岛素值,其中有家族史初诊2型糖尿病患者(FH+DM)61例、无家族史初诊2型糖尿病患者(FH-DM)55例、有家族史正常糖耐量者(FH+)31例、无家族史正常糖耐量者(FH-)54例.以HOMA胰岛素抵抗指数(HOMA-IR)评价胰岛素抵抗.结果 校正性别、年龄、BMI后,(1)糖尿病组(FH+DM和FH-DM)TC、TG、空腹血浆血糖(FPG)、糖负荷后2 h血糖、空腹胰岛素(Fins)、HOMA-IR明显高于糖耐量正常组(FH+和FH-),胰岛素峰值倍数明显低于糖耐量正常组,P<0.05;(2)4组胰岛素均2 min达分泌峰值,4 min开始下降;(3)FH+组胰岛素峰值倍数较FH-组下降20.8%,分别为7.27与9.18倍,P<0.05;(4)FH+DM组2 min胰岛素分泌峰值、HOMA-IR、患病年龄明显低于FH-DM组(P<0.05),两组峰值倍数分别为5.18与5.31倍,差异无统计学意义(P>0.05);(5)FH+DM组胰岛素峰值倍数较FH-组下降了 43.6%(P<0.05).结论 2型糖尿病早期,尽管胰岛素抵抗表现不显著,遗传背景却使胰岛β细胞第一时相分泌功能减退;而无遗传背景者,胰岛素抵抗使胰岛素第一时相分泌下降相对缓慢.     

精氨酸刺激试验在不同糖代谢状态人群的临床应用

目的探讨精氨酸刺激试验能否用于评价胰岛β细胞储备功能及其判断标准。方法分别检测225人空腹及盐酸精氨酸刺激后2、4、6 min时血糖(PG)、真胰岛素(TI)、C肽(CP)水平的变化,其中正常糖耐量组(NGT)39名、糖耐量受损组(IGT)29例、1型糖尿病组(T1DM)11例,新诊断2型糖尿病组(NT2DM)43例和原诊断2型糖尿病组(PT2DM)103例。结果(1)NGT组空腹TI/PG显著高于IGT组(P<0.05),但两组的空腹CP/PG差异无统计学意义(P>0.05)。空腹CP/PG在T1DM、NT2DM、PT2DM组显著低于NGT、IGT组(均P<0.01),并且PT2DM组显著低于NT2DM组(P<0.01)。(2)精氨酸刺激后T1DM组无快速TI、CP分泌。其余各组在刺激后TI/PG、CP/PG除IGT组与NGT组差异无统计学意义(P>0.05)外,NT2DM、TP2DM组均显著低于NGT、IGT组(均P<0.01),并且2 min时PT2DM组亦显著低于NT2DM组(均P<0.01)。(3)精氨酸刺激后TI/PG、CP/PG的增值及曲线下面积在NGT、NT2DM、PT2DM三组间差异有统计学意义(均P<0.01)。结论(1)精氨酸刺激试验可用于判别和评估不同糖代谢状态人群胰岛β细胞功能,尤其是DM人群β细胞功能的判别。(2)精氨酸刺激后TI/PG值及其峰值/空腹值、TI/PG的增值和曲线下面积均可能作为评价β细胞功能异常的指标,其中以TI/PG的增值和曲线下面积为佳。     

胰岛自身抗体与β细胞功能关系的研究

目的分析胰岛自身抗体与β细胞功能关系,探讨胰岛细胞抗体(ICA)、谷氨酸脱羧酶抗体(GADA)在类似2型糖尿病的成人隐匿性自身免疫糖尿病(LADA)中的诊断价值,指导临床糖尿病分型诊断和治疗。方法初诊2型糖尿病病人70例,正常糖耐量者70例,测定ICA、GADA及胰岛素释放,计算胰岛素分泌指数(HOMA-IS)、胰岛素抵抗指数(HOMA-IR)及ICA、GADA阳性率。初诊2型糖尿病自身抗体阳性组与阴性组进行年龄、体重指数(BMI)、腰臀比值(WHR)、糖化血红蛋白(HbA1c)、空腹和餐后2h胰岛素(FINS、餐后2hINS2h)、HOMA-IS及HOMA-IR等临床特征比较。结果初诊2型糖尿病组ICA阳性率为11.4%,正常糖耐量组为0.0%(P<0.01);GADA阳性率在糖尿病组为18.6%,正常糖耐量组为4.3%(P<0.01)。空腹及餐后2h胰岛素在抗体阳性组明显低于阴性组(P<0.001);HOMA-IS指数及HOMA-IR指数在抗体阴性组、抗体单阳性组及双阳性组依次降低。结论临床诊断为2型DM病人中可能有LADA病人,抗体阳性者胰岛功能明显低于抗体阴性者,提示其胰岛功能有明显损伤,而抗体阴性组胰岛素抵抗明显,提示胰岛自身抗体结合胰岛β细胞功能对LADA病人早期诊断有帮助。     

Immunologic and genetic aspects of latent autoimmune diabetes in the adult

The presence of islet cell autoantibodies (ICA), and especially of glutamic acid decarboxylase autoantibodies (GAD65Ab), in patients with non-insulin-dependent diabetes mellitus identifies the so-called latent autoimmune diabetes in the adult (LADA). LADA patients have an increased risk for developing insulin deficiency, and in 60-80% of cases the exogenous insulin therapy must be started within 5-6 years. GAD65Ab identify a subgroup of type 2 diabetic (T2DM) patients with low body mass index (BMI) at the time of diagnosis. The presence of GAD65Ab at high titres and directed against COOH-terminal epitopes of the autoantigen, or the presence of both GAD65Ab and ICA, discriminates patients with clinical characteristics very similar to those of a slowly progressive form of type 1 diabetes (T1DM). On the other hand, the presence of low levels GAD65Ab, in the absence of ICA or other immune markers, such as IA-2 antibodies, characterizes a subgroup of patients with clinical characteristics almost indistinguishable from those of typical T2DM patients. The autoimmune origin of LADA is also demonstrated by the increased frequency of thyroid and adrenal autoantibodies, as compared to GAD65Ab-negative T2DM patients, and by the strong genetic association with HLA-DR3-DQ2, -DR4-DQ8 and the polymorphisms of the MHC class I chain-related A (MICA) and CTLA-4 genes. Metabolic studies have shown the coexistence of insulin resistance and insulin secretion defect supporting the hypothesis that LADA may be the result of the interaction of a genetic background predisposing for islet autoimmunity and a genetic background predisposing for T2DM.     

成年人迟发性自身免疫性糖尿病的临床特征

探讨成年人迟发性自身免疫性糖尿病的临床特征,以期早期识别。方法对４１８例临床诊断为２型糖尿病的患者通过ＩＣＡ和ＧＡＤ抗体测定,筛出ＬＡＤＡ５２例,与３０例成人速发型１型糖悄病和５０例健康人比较。结论目前简易可行的鉴别方法是检测免疫学指标ＩＣＡ和／或ＧＡＤ抗体,从２型糖尿病中筛查出ＬＡＤＡ。     

羧基肽酶-H抗体对成人隐匿性自身免疫糖尿病的诊断意义

目的 探讨羧基肽酶—H自身抗体(CPH—Ab)阳性的2型糖尿病(T2DM)患者的临床特征及该抗体对成人隐匿性自身免疫糖尿病(LADA)的诊断价值。方法 选择临床初诊为T2DM患者545例，1型糖尿病(T1DM)患者85例，健康对照123例进行CPH—Ab测定，同时检测T2DM患者谷氨酸脱羧酶抗体(GAD—Ab)。比较各组CPH—Ab的阳性率以及T2DM中依据CPH—Ab、GAD—Ab划分的3组患者的临床特点。采用放射免疫沉淀法检测CPH—Ab和GAD—Ab。结果 CPH—Ab阳性率在T2DM患者(5．5％，30／545)高于T1DM患者(0％，0／85)和正常对照(0．8％，1／123)(P＜0．05)，30例CPH—Ab阳性的T2DM患者只有1例同时GAD—Ab阳性。CPH—Ab在低体重(BMI＜21kg／m^2)者中的阳性率较高，且该抗体阳性的患者具有起病年龄跨度大、病程较长、低体重、易发生酮症等特点，其空腹C肽介于GAD—Ab阳性与两种抗体(GAD—Ab和CPH—Ab)均阴性的T2DM患者之间，反映代谢综合征的指标水平较低(包括较低的BMI、血压和甘油三酯)，而周围神经病变的比例较高。结论 CPH—Ab阳性糖尿病患者的临床特点介于经典的LADA(GAD—Ab阳性)与T2DM患者间。CPH抗体检测是LADA诊断的一项新指标。     

Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients

Insulin resistance is a primary component in the pathophysiology of type 2 diabetes. In latent autoimmune diabetes in adults (LADA), insulin resistance has been reported to be significantly lower than in autoantibody-negative type 2 diabetes (T2DM), but whether this might be related to differences in body mass index (BMI) has not been excluded. Furthermore, previous studies have used limiting inclusive criteria for LADA, requiring only the presence of GADA or IA-2A. To apply more inclusive criteria for LADA, consistent with recent recommendations, we defined LADA by clinical manifestations characteristic of T2DM, but with the presence of any combination of GADA, IA-2A, ICA, or IAA. We recruited 43 LADA patients, 70 T2DM patients, and 150 non-diabetic controls. Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index, and BMI was calculated. We found that insulin resistance in LADA is equivalent to that of T2DM. When insulin resistance is assessed as a function of BMI, both diabetic populations demonstrated an insulin resistance equally greater than normal controls. The interaction between insulin resistance and BMI in the two diabetic groups was significantly different from that demonstrated in non-diabetic controls. In summary, LADA demonstrates insulin resistance of similar magnitude to T2DM, but with the concurrent component of an immune attack against the pancreatic beta-cells. LADA patients may be at significant risk for metabolic consequences of insulin resistance other than glucose metabolism, such as those described in the metabolic syndrome. As complications and treatment regimens specific to LADA are realized, improved means of identification of LADA will become increasingly important.     

谷氨酸脱羧酶抗体诊断成人隐匿性自身免疫性糖尿病探讨

采用放射配体法检测谷氨酸脱羧酶（ＧＡＤ６５）抗体，对１９５例≥３５岁非酮症Ⅱ型糖尿病起病半年以上者和４５例正常对照者的观察表明：本组Ⅱ型糖尿病者ＧＡＤ６５抗体阳性率为１４．８％，高于正常对照者的２．２％；发病年龄〈４０岁、有酮症史、体重指数（ＢＭＩ）〈２１ｋｇ／ｍ＾２、空腹血清Ｃ肽〈０．３ｎｍｏｌ／Ｌ和（或）胰升糖素刺激后６分钟血清Ｃ肽〈０．６ｎｍｏｌ／Ｌ者，ＧＡＤ６５抗体阳性率均高于相应对照组（     

Metabolic syndrome in adult-onset latent autoimmune diabetes

Background. Latent autoimmune diabetes in adults (LADA) is characterized by islet beta-cell loss and absolute insulin deficiency, however, studies in recent years have shown some extent of insulin resistance in LADA patients. In view of insulin resistance being the central pathogenesis of metabolic syndrome (MS), we hypothesized that MS could be found in LADA patients. Methods. A total of 60 glutamic acid decarboxylase antibody (GAD-Ab)-positive LADA patients and 120 patients with type 2 diabetes (T2DM) were enrolled for the study. MS and its components were diagnosed according to the working definitions proposed by World Health Organization and National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III [ATP III]). Insulin resistance and high sensitive C reactive protein (hsCRP) levels were also evaluated in patients with or without MS. Serum insulin and hsCRP levels were determined with radioimmune and immunoturbidimetric assays, respectively. Results. MS was found in 50% of LADA patients by WHO criteria and in 40% by ATP III criteria. The proportions of MS and its metabolic components were all comparable between LADA and T2DM patients except that a lower proportion of hypertension was seen in LADA. LADA patients with MS had significantly higher HOMA-IR index (0.85 +/- 0.33 vs. 0.60 +/- 0.26, p = 0.001 for WHO criteria; 0.89 +/- 0.34 vs. 0.62 +/- 0.26, p = 0.000 for ATP III criteria) and hsCRP levels (0.86 vs. 0.41, p = 0.019 for WHO criteria; 0.96 vs. 0.66, p = 0.018 for ATP III criteria) than LADA without MS patients. Conclusions. Our findings indicate that MS does exist in LADA patients, suggesting that the a diagnosis of MS could not exclude one of LADA and that insulin sensitizers may be beneficial in therapeutic strategies for treating these conditions.     

Epitope analysis of GAD65 autoantibodies in adult-onset type 1 diabetes and latent autoimmune diabetes in adults with thyroid autoimmunity

This study aimed at determining which GAD65 epitopes the spontaneous antibodies recognized and whether the epitope-specific GAD65Abs could be associated with the development of thyroid autoimmunity in Chinese adult-onset type 1 diabetes (T1DM) and latent autoimmune diabetes in adults (LADA). The levels of GAD65Abs and their reactivities to N-terminal (GAD65-N), middle (GAD65-M) and C-terminal (GAD65-C) regions of human GAD65 were measured by radioligand assay in 109 patients with adult-onset T1DM and 107 with LADA. TPOAb, TGAb and the genotypes of HLADQA1-DQB1 were determined. The percentage of LADA patients with GAD65-NAb was significantly higher than that of adult-onset T1DM patients (21.5% vs. 11.0%, P = 0.037), but LADA patients with GAD65-CAb less than T1DM patients (47.7% vs. 70.6%, P = 0.001). LADA patients with both GAD65-M and GAD65-CAb (GAD65-M + CAb) appeared to be at higher risk for the development of thyroid autoimmunity, lower serum C-peptide level and the requirement for insulin therapy (P < 0.05). More frequent T1DM patients with HLADQA1*03-DQB1*0303 developed GAD65-M + CAb (55.8% vs. 35.1%, P = 0.008). In comparison with those without thyroid autoimmunity, more frequent T1DM patients and LADA patients with thyroid autoimmunity displayed GAD65-M + CAbs (44.0% vs.16.9% and 53.1% vs. 17.3%, P = 0.002 and <0.001, respectively) with a diagnostic specificity of 83.1 or 82.7% for thyroid autoimmunity, respectively. LADA patients with GAD65-M + CAbs had clinical features similar to T1DM patients. Adult-onset T1DM and LADA patients with GAD65-M + CAbs are at an increased risk for the development of thyroid autoimmunity.     

HLA-associated cellular response to GAD in type 2 diabetes with antibodies to GAD

Proliferative response of peripheral blood mononuclear cells (PBMC) to glutamic acid decarboxylase (GAD), which has been reported in patients with type 1 diabetes, was measured in type 2 diabetes, especially in patients with antibodies to GAD initially diagnosed as having type 2 diabetes (anti-GAD+ type 2 diabetes). We studied 12 patients with type 1 diabetes, 22 with anti-GAD+ type 2 diabetes, 31 with type 2 diabetes who were negative for anti-GAD (anti-GAD+ type 2 diabetes), and 30 healthy control subjects for cellular responses in vitro to GAD. The mean stimulation index (SI) in response to GAD was significantly higher in type 1 diabetes than in anti-GAD+ type 2 diabetes or healthy controls (1.47+/-0.35 vs. 1.11+/-0.35, P<0.05, and 1.06+/-0.07, P<0.05, respectively). The mean     

The relationship between peripheral T cell reactivity to insulin, clinical remissions and cytokine production in type 1 (insulin-dependent) diabetes mellitus.

Antigenic proliferative responses of peripheral blood mononuclear cells (PBMC) to insulin were studied in 44 type 1 new-onset diabetic subjects. Of them, 14 (32%) had a stimulation index (> or =3) above the mean + 3 SD of 39 healthy controls and of 7 of 15 (47%) diabetic patients of long duration (P = 0.001). Responses to insulin were not dictated by specific major histocompatibility complex class II association and were not observed in normal subjects with diabetes-associated human leukocyte antigen-DR/DQ alleles. Whereas no relation of PBMC reactivity with insulin autoantibodies was found, there was a positive correlation with the presence of at least one of the four autoantibodies tested and with IA-2 antibody. An interesting finding was that the proportion of patients with subsequent low insulin requirement, up to 24 months, was significantly higher in patients who showed PBMC reactivity to insulin (8 of 8) than in those who did not (10 of 24, 42%; P = 0.004). The former had a higher mean stimulation index than the latter (3.3+/-2.6 vs. 1.5+/-0.6; P = 0.006). Furthermore, interleukin-4 (IL-4) production was lower in type 1 diabetic patients who proliferated to insulin than in those who did not (23+/-15 vs. 64+/-47 pg/mL; P = 0.04), but interferon-gamma, IL-2, and IL-10 productions were similar. In conclusion, these results suggest that proliferation to insulin may reflect the presence of an higher residual beta-cell mass.     

2型糖尿病和非酒精性脂肪肝病患者的胰岛素抵抗和胰岛β细胞功能

目的 探讨2型糖尿病(T2DM)和非酒精性脂肪肝病(NAFLD)患者胰岛β细胞功能和胰岛素抵抗的特征.方法 206例研究对象根据是否有T2DM和NAFLD分为4组,采用肝脏胰岛素抵抗指数(HIR)、HOMA胰岛素抵抗指数(HOMA-IR)及Matsuda指数(MSI)评估胰岛素抵抗性,采用HOMA-β、早相及晚相胰岛素分泌指数评估胰岛β细胞功能.结果 NAFLD组和T2DM伴NAFLD组的HIR均显著高于对照组和T2DM组(4.13±0.64,4.03±0.69比3.52±0.78,3.53±0.64,P<0.05),T2DM伴NAFLD组的HOMA-IR显著高于T2DM和NAFLD组(3.35±2.69比2.31±1.39,2.40±1.55,P<0.05);NAFLD组的早相胰岛素分泌指标显著低于对照组(2.13±0.17比2.61±0.13,P<0.05),而T2DM组和T2DM伴NAFLD组的HOMA-β、早相及晚相胰岛素分泌指标均明显低于对照组(P<0.05).结论 NAFLD患者主要表现为肝脏胰岛素抵抗,其胰岛β细胞早相胰岛素分泌受损;T2DM患者存在胰岛素抵抗,其胰岛β细胞早、晚相胰岛素分泌功能均受损.当患者既有T2DM又有NAFLD时,胰岛素抵抗将更严重.