血糖调节异常者胰岛素抵抗及胰岛β细胞功能研究

目的研究胰岛素抵抗和胰岛β细胞功能与中国人血糖调节异常(IGR)的关系。方法根据口服葡萄糖耐量试验(OGTT)将209例受试者分为正常糖耐量(NGT)组、空腹血糖受损(IFG)组、糖耐量减退(IGT)组、IFG/IGT组和糖尿病(DM)患者组,用胰岛素敏感指数(ISI-COM)评价胰岛素抵抗(IR),用调整β细胞功能指数(modifiedβcell function index,MBCI)评价β细胞功能,并用早期胰岛分泌指数(△I30/△G30)评价急性期胰岛分泌功能,OGTT胰岛素曲线下面积评价二相期胰岛素分泌功能。结果IGR各组与DM组ISI-COM较NGT组有显著降低,差异有统计学意义(P0.01),而IGR各组间差异无统计学意义(P0.05)。IFG组和IGT组β细胞功能较NGT组显著降低,差异有统计学意义(P0.01),而IFG/IGT组与DM组间差异无统计学意义(P0.05)。各病例组早期胰岛分泌功能亦较NGT组有显著性降低,差异有统计学意义(P0.01),IGT组与IFG组间差异也有统计学意义(P0.01)。结论IGR各阶段均存在不同程度的IR和β细胞功能异常,其中IFG和IGT有不同的发病机制和过程,提示对于不同糖代谢异常的患者需要不同的治疗方式,以延缓血糖代谢异常的进展。     

糖代谢异常患者胰岛素抵抗和胰岛β细胞功能与血清高半胱氨酸的相关性分析

摘要:目的：探讨糖代谢异常人群胰岛素抵抗和胰岛β细胞功能与高半胱氨酸(Hcy)的关系。 方法：对67例糖耐量正常（NGT）者及104例糖耐量受损（IGT）、58例空腹血糖调节受损（IFG）、109例2型糖尿病（T2DM）患者,检测空腹血糖（FPG）、口服葡萄糖耐量试验（OGTT) 2 h血糖、Hcy及空腹胰岛素水平,计算稳态模型评估胰岛素抵抗指数(HOMA-IR)、HOMA胰岛β细胞功能指数(HBCI)、空腹胰岛β细胞功能指数(FBCI)。 结果：与NGT、IFG组比较,IGT组HOMA-IR、HBCI、Hcy差异有统计学意义（P均<0.05）;与NGT、IFG、IGT组比较,T2DM组HOMA-IR、HBCI、FBCI、Hcy差异有统计学意义（P均＜0.05）。Hcy与HOMA-IR呈正相关（r=0.233,P<0.05）,与HBCI、FBCI呈负相关（r分别为－0.354、－0.289,P均<0.05）。 结论：Hcy与葡萄糖代谢异常有相关性,可作为评价胰岛素抵抗、胰岛β细胞分泌功能受损的一项观察指标。     

糖尿病前期患者血清脂联素和超敏C反应蛋白水平分析

目的探讨血清脂联素、超敏C反应蛋白(hs-CRP)水平变化与糖尿病前期发生的危险因素的关系。方法选取健康对照组(NGT)、糖耐量减低组(IGT)、空腹血糖受损合并糖耐量减低组(IFG/IGT)各100例,测定各受试者血清脂联素、hs-CRP、空腹胰岛素、空腹血糖、餐后2 h血糖,应用稳态模型评估法评价胰岛素抵抗。结果 IGT组、IFG/IGT组血清脂联素均显著低于NGT组(P<0.01),IFG/IGT组的脂联素水平低于单纯IGT组(P<0.05)。脂联素水平与空腹血糖、餐后2 h血糖、胰岛素抵抗指数(HOMA-IR)呈负相关(P值均小于0.01)。单纯IGT组、IFG/IGT组血清hs-CRP水平明显高于NGT组(P<0.01),IFG/IGT组血清hs-CRP水平高于单纯IGT组(P<0.05)。血清hs-CRP水平与空腹血糖、餐后2 h血糖、HOMA-IR呈正相关(P值均小于0.01)。结论血清脂联素、hs-CRP可能是加重糖尿病前期胰岛素抵抗的危险因素,糖调节受损期即可能存在慢性低度炎症反应。在糖尿病前期,脂联素、hs-CRP可能参与了糖尿病的发生及发展。     

腹型肥胖人群中不同糖代谢水平者胰岛素抵抗及胰岛分泌功能的探讨

目的 探讨腹型肥胖人群中不同糖代谢水平者胰岛素抵抗及胰岛分泌功能的状态。方法 腹型肥胖患者共382例，其中正常糖耐量(NGT)组251例，空腹血糖异常(IFG)组40例，异常糖耐量(IGT)组41例，2型糖尿病(DM组)50例。测腰围、血压、空腹血脂、血糖及血浆胰岛素，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B细胞功能指数(HBCI)作为胰岛素分泌指标。结果 在腹型肥胖的人群中，不同糖代谢组的HOMA-IR差异具有统计学意义，从NGT→IFG／IGT→DM组HOMA-IR逐渐升高，而HBCI在各组内变化较大，数值分布较分散，与NGT、IFG、IGT组相比，DM组的HBCI明显下降，差别有统计学意义。同时收缩压随着糖代谢的恶化从NGT、IGT IFG到DM组逐步升高，舒张压的变化无明显的规律。结论 腹型肥胖人群中，从NGT经IFG／IGT向2型糖尿病发展的过程中，胰岛素敏感性逐渐下降，β细胞胰岛素分泌功能明显下降是出现DM的主要原因。这一结果与其他种族中的研究结果不完全相同，提示即使是肥胖相关的2型糖尿病，种族、遗传因素仍然在糖尿病发展过程中发挥着重要作用。     

糖耐量低减患者血清超灵敏C反应蛋白水平与胰岛素抵抗

目的:探讨糖耐量低减患者(impairedglucosetolerance,IGT)血清超灵敏C反应蛋白highsensitiveCreactiveprotein,hs-CRP水平与机体胰岛素()敏感性和胰岛素分泌功能的关系。方法:选择2001-01/2003-04在解放军第一军医大学南方医院内分泌住院和门诊的IGT患者50例为研究对象,根据是否合并空腹血糖受损(impairedfastingglucose,IFG)将患者分为合并IFG的IGT组(非单纯IGT组)和未合并IFG的IGT组(单纯IGT组)。选择本院同期体检自愿者或患者家属20例作为对照组。运用高灵敏酶联免疫吸附法检测两组研究对象血清hs-CRP水平,同时检测血糖、血清胰岛素、糖化血红蛋白,并计算稳态模型分析胰岛素抵抗指数(HOMA-IR和稳态模型分析胰岛β细胞分泌)指数(HOMA-IS)以反映胰岛素敏感性和胰岛细胞功能。结果:非单纯IGT组和单纯IGT组患者的血清hs-CRP水平犤(3.02±1.09),(1.72±0.87)mg/L犦显著高于对照组犤(0.81±0.45)mg/L犦(q=8.33,3.79,P<0.01);HOMA-IR明显高于对照组(q=13.93,9.79,P<0.01)和HOMA-IS明显低于对照组(q=12.80,9.38,P<0.01)。非单纯IGT组患者血清hs-CRP水平和HOMA-IR显著高于单纯IGT组(q=4.09,4.89,P<0.01),而HOMA-IS明显低于单纯IGT组(q=3.85,P<0.01)。线性相关分析显示,IGT患者的血清hs-CRP水平均与糖化血红蛋     

阻塞性睡眠呼吸暂停综合征患者的胰岛素分泌情况

目的评价阻塞性睡眠呼吸暂停综合征（OSAS）患者,在正常糖耐量（NGT）时,胰岛β细胞功能和胰岛素抵抗情况。方法选择35例OSAS正常糖耐量（NGT）患者和22例非OSAS非NGT对照者,全部行口服葡萄糖耐量试验,计算早时相胰岛素生成指数△I30/G△30和胰岛素抵抗指数（HOMA-IR）。结果 OSAS正常糖耐量（NGT）患者的△I30/△G30是11.1±5.2;HOMA-IR是5.3±1.2。对照组非OSAS非NGT△I30/△G30是28.3±10.2;HOMA-IR是4.0±3.5。结论 OSAS患者存在胰岛素早期分泌功能缺陷和胰岛素抵抗。     

糖耐量减退病人的代谢特征分析

目的 探讨糖耐量减退(IGT)病人胰岛素抵抗、β细胞功能及相关的代谢改善。方法 对45例正常人(NGT组)和78例IGT病人口服葡萄糖耐量试验(OGTT)和胰岛素释放试验,并测定其血脂、尿酸、血压和体重指数(BMI)。结果 与NGT组相比,IGT组胰岛素敏感指数(P<0.01)和初期胰岛素分泌指数明显降低(P<0.01),OGTT各时相胰岛素之和曼著升高(P<0.05),胰岛素敏感指数依次与BMI、TG、HDL-C和血糖相关;IGT病人TG、尿酸、收缩压、舒张压和BMI明显增高,HDL-C显著降低(P<0.05)。结论 IGT病人存在明显的胰岛素抵抗、胰岛β细胞功能异常并伴有多种代谢异常。     

糖耐量减低者胰岛素抵抗、胰岛B细胞功能及相关代谢指标分析

目的分析糖耐量减低者的胰岛素抵抗、胰岛B细胞功能及相关代谢指标。方法根据口服葡萄糖耐量试验(OGTT),将243例入选者分为糖耐量减低组(IGT组,108例)及糖耐量正常组(NGT组,135例),测定空腹及服糖后2小时胰岛素(2 hINS)、空腹甘油三酯(TG)、胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、游离脂肪酸(FFA),计算胰岛素抵抗指数(HOMA-IR)、胰岛素分泌指数(HOMA-β)及葡萄糖处置指数(DI)。结果①IGT组HOMA-IR水平显著高于NGT组(0.56±0.25 vs 0.40±0.20,P<0.01);②IGT组DI水平显著低于NGT组(1.66±0.16 vs 2.66±0.21,P<0.01);③IGT组TG、FFA、FINS2、hINS显著高于NGT组(P<0.01),HDL-C显著低于NGT组(P<0.01);两组间TC、LDL-C、HOMA-β差异无统计学意义(P>0.05)。结论糖耐量减低者以胰岛素抵抗及高胰岛素血症为主,脂毒性在这一过程中起重要作用。     

瘦素与老年患者胰岛素抵抗和胰岛功能的相关性

目的:探讨瘦素是否与老年患者包括临床糖尿病(DM)、糖耐量减低(IGT)、空腹血糖调节受损(IFG)类型胰岛素抵抗和胰岛功能等指标相关联.方法:选择临床2型糖尿病患者40例(T2DM组),IGT患者30例(IGT组),IFG患者30例(IFG组)和正常对照组30例,检测各组循环瘦素、胆固醇、甘油三酯、高密度脂蛋白胆固醇、空腹血糖(FPG)、餐后2 h血糖、空腹胰岛素(FINs)、餐后2 h胰岛素、糖化血红蛋白(HbA1c)、C-肽等指标,用稳态模式(Homa Model)公式评估胰岛素抵抗指数(HOMA-IR)和胰岛β细胞功能指数.结果:T2DM组、IGT组和IFG组瘦素水平(*9滋g)分别为4.27 ± 1.82、4.15 ± 1.96、4.19 ± 1.9,高于正常对照组的2.43 ± 0.31;HOMA-IR数值分别为3.48 ± 0.84、3.01 ± 0.67、3.24 ± 0.26,高于正常对照组的1.23 ± 0.42;FINs、FPG、C-肽、HbA1c均高于正常对照组(P ＜ 0.01);T2DM组、IGT组和IFG组在校正胰岛素抵抗后的胰岛细胞功能分别为178 ± 49、165 ± 59、170 ± 52,低于正常对照组的346 ± 54.多元逐步回归分析显示:FPG、FINS、C-肽、HbA1c、瘦素水平是影响HOMA-IR的独立危险因素.结论:老年患者循环瘦素水平的升高是胰岛素抵抗和胰岛*9茁细胞功能缺陷的危险因素.     

糖调节受损的胰岛素抵抗及β细胞功能的研究

目的 探讨不同糖调节状态的β细胞功能与胰岛素抵抗（IR）的关系.方法 （1）对我院2007年健康体检的在职干部,选取正常糖耐量（NGT） 122例、空腹血糖受损（IFG） 39例、糖耐量减低（IGT） 64例、新诊断2型糖尿病（T2DM）72例,共4组不同糖调节状态人群.（2）检测空腹及糖负荷后30 min和2h的血糖（PG）、血浆胰岛素（FIns）.（3）采用HOMA-IR评价IR,HOMA-β及ΔⅠ30/ΔG30分别评价基础状态下及糖负荷后的早时相胰岛β细胞功能.结果 NGT、IFG、IGT和糖尿病组HOMA-IR依次增高,分别为：1.52（0.96 ～2.37）、1.62（1.17 ～2.60）、1.65（1.22 ～2.82）、3.12（1.50 ～4.41）;而ΔⅠ30/ΔG30逐渐降低,分别为：16.42（10.13 ～22.71）mU/mmol、9.45 （5.65 ～ 15.74） mU/mmol、7.36（5.73 ～ 19.13） mU/mmol、3.86（2.13 ～5.96） mU/mmol.HOMA-β按NGT、IFG、IGT、糖尿病逐渐降低,分别为：72.74（42.7 ～ 111.8） mU/mmol、65.72（52.5 ～ 124.0）mU/mmol、50.39 （21.2 ～ 77.5） mU/mmol、39.10 （26.7 ～ 63.2） mU/mmol;4组人群HOMA-IR、HOMA-β及ΔⅠ30/ΔG30均差异显著（P ＜0.0001）.HOMA-IR：糖尿病组明显高于其他组（P＜0.05）,而其他组之间无明显差别（P＞0.05）.HOMA-β：IGT组明显低于IFG及NGT组（P＜0.05）.ΔⅠ30/ΔG30：糖尿病组均明显低于其余三组（P＜0.05）.结论 IFG患者空腹血糖升高可能主要由于基础β细胞功能缺陷所致.糖负荷后的糖调节能力可能主要与IR、早时相胰岛素分泌缺陷有关.     

探讨糖尿病前期患者血浆IL-18、PAI-1水平变化与胰岛素抵抗的相关性

目的探讨血浆白细胞介素-18(IL-18)、纤溶酶原激活物抑制物-1(PAI-1)水平变化与Ⅱ型糖尿病发病危险因素的关系.方法 设立健康人对照(NGT)组、糖耐量减低( IGT )组、空腹血糖受损合并糖耐量减低(IFG/IGT)组,每组各100例.测定各受试者血浆 IL-18、PAI-1、血清空腹胰岛素、空腹血糖、餐后2 h血糖,应用稳态模型评估法评价胰岛素抵抗(HOMA-IR).结果 IGT组、IFG/IGT组血浆 IL-18、PAI-1 水平均高于NGT组(P<0.01).IFG/IGT组血浆 IL-18、PAI-1 水平均高于IGT组(P<0.05).相关分析显示IL-18、PAI-1 水平与空腹血糖、餐后2 h血糖、HOMA-IR呈正相关(P<0.01).结论血浆 IL-18、PAI-1 水平升高可能是加重糖尿病前期患者胰岛素抵抗的危险因素;在糖尿病前期,IL-18、PAI-1可能参与了Ⅱ型糖尿病的发生、发展.     

Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans

OBJECTIVE: To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS: We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of beta-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS: Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased approximately 30% (P < 0.05), but clamp-determined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced approximately 35% (P < 0.002) and approximately 30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but approximately 15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced approximately 30%. IFG/NGT differed from NFG/IGT by having approximately 40% lower HOMA-%B (P < 0.012) and approximately 50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS: Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity.     

Contribution of insulin-stimulated glucose uptake and basal hepatic insulin sensitivity to surrogate measures of insulin sensitivity

OBJECTIVE: The goal of this study was to evaluate the performance of surrogate measures of insulin sensitivity and insulin secretion. RESEARCH DESIGN AND METHODS: The homeostasis model assessment (HOMA) of insulin resistance (IR) and the insulin sensitivity index (S(i)) from oral glucose tolerance test (OGTT) were compared with the M value from a hyperinsulinemic-euglycemic clamp in 467 subjects with various degrees of glucose tolerance. Endogenous glucose production (EGP) and hepatic insulin sensitivity were determined in a subset (n = 143). Insulin secretion was estimated as the HOMA beta-cell index and as the insulinogenic index from the first 30 min of the OGTT (I/G30) and compared with the first-phase insulin response (FPIR) to an intravenous glucose tolerance test (n = 218). RESULTS: The M value correlated with the HOMA-IR (r = -0.591, P < 0.0001) and the S(i) (r = 0.533, P < 0.0001) indexes in the total study group. HOMA-IR correlated with basal EGP in the total study group (r = 0.378, P < 0.0005) and in subjects with diabetes (r = 0.330, P = 0.01). However, neither HOMA-IR nor S(i) correlated significantly with the M value in subjects with impaired fasting glucose (IFG) (r = -0.108, P = 0.5; r = 0.01, P = 0.9) or IFG/impaired glucose tolerance (IGT) (r = -0.167, P = 0.4; r = 0.09, P = 0.6). The HOMA-IR correlated with hepatic insulin sensitivity in the whole study group (r = -0.395, P < 0.005) as well as in the IFG/IGT subgroup (r = -0.634, P = 0.002) and in the diabetic subgroup (r = -0.348, P = 0.008). In subjects with IFG/IGT, hepatic insulin sensitivity was the most important determinant of HOMA-IR, explaining 40% of its variation. The HOMA beta-cell index showed a weak correlation with FPIR in the whole study group (r = 0.294, P = 0.001) but not in the subgroups. In contrast, the I/G30 correlated with FPIR in the whole study group (r = 0.472, P < 0.0005) and in the IFG/IGT subgroup (r = 0.493, P < 0.005). CONCLUSIONS: HOMA-IR is dependent upon both peripheral and hepatic insulin sensitivity, the contribution of which differs between subjects with normal and elevated fasting glucose concentrations. These discrepancies develop as a consequence of a nonparallel deterioration of the variables included in the equations with worsening of glucose tolerance.     

糖耐量受损者胰岛素抵抗和β细胞功能的研究

目的　探讨糖耐量受损 (IGT)患者胰岛素抵抗、β细胞功能和相关的代谢改变。 方法　对 6 4例血糖正常者 (NGT)和 97例IGT患者进行口服葡萄糖耐量试验 (OGTT)、胰岛素释放试验 ,并测定其血脂、血压、体重指数 (BMI)和腰臀比值 (WHR)。结果　与NGT组比较 ,IGT组空腹胰岛素水平、OGTT后胰岛素曲线下面积显著升高 (P <0 0 5 ) ;胰岛素敏感指数、初期胰岛素分泌指数明显降低 (P <0 0 1) ;胰岛素敏感指数依次与腰臀比值、BMI、甘油三脂 (TG)、高密度脂蛋白 胆固醇 (HDL C)、空腹血糖和舒张压相关 ;IGT患者TG、舒张压、收缩压、BMI和腰臀比值明显增高 ,HDL C明显降低。结论　IGT患者存在胰岛素抵抗和 β细胞功能异常并伴有多种代谢紊乱。     

孕妇在不同糖耐量状态下超敏C-反应蛋白与胰岛素抵抗相关性研究

目的 研究孕妇在不同糖耐量状态下血清超敏C-反应蛋白(hs-CRP)与胰岛素抵抗(IR)的关系.方法 孕妇孕24～28周行50 g口服葡萄糖负荷试验,阳性者再行75 g口服葡萄糖耐量试验,根据血糖结果分为妊娠糖尿病组41例、糖耐量减低组30例和糖耐量正常组27例,用ELISA方法测定hs-CRP水平,同时计算稳态模式胰岛素抵抗指数(HOMA-IR)、稳态模式胰岛B细胞功能指数(HBCI)和30 min净增胰岛素/30 min净增血糖(△I30/△G30).结果 ①从糖耐量正常组到糖耐量减低组到妊娠糖尿病组,hs-CRP [(6.15±2.63)、(7.65±4.27)、(10.80 ±3.57)mg/L,F=5.628,P=0.021]、HOMA-IR(2.54±0.74、3.51±0.29、3.96 ±2.16,F=6.928,P=0.011)呈递增趋势,而HBCI(426.08±89.85、266.69±203.32、223.82 ±148.58,F=4.283,P:0.043)和△I30/△G30(27.90±19.22、15.12±12.50、13.13 ±12.98,F=6.505,P=0.014)呈递减倾向;②Pearson相关分析显示孕前BMI、空腹胰岛素(Fins)、hs-CRP与HOMA-IR正相关(r=0.320、0.833、0.288,P均＜0.01);多元回归分析显示,孕前BMI、FBG、Fins、hs-CRP是影响HOMA-IR的显著因素(回归系数分别为0.320、0.340、0.709、0.288,R2=0.92,P均＜0.01).结论 妊娠糖尿病患者的血清hs-CRP水平为影响IR的显著因素,提示hs-CRP可能通过多种机制加重IR,参与妊娠糖尿病的发病.     

不同年龄段的正常糖耐量人群血糖值及其相关因素分析

目的 分析不同年龄段正常糖耐量(NGT)者血糖水平及相互关系.方法 选择上海市杨浦区部分街道流行病学调研2098例30岁以上居民,根据糖耐量(OGTT)检测中空腹血糖值(FPG)和2 h血糖值(2 hPG),诊断为NGT、糖耐量低减(IGT)、空腹血糖受损(IFG)、IGT合并IFG(IGT/IFG)、糖尿病(DM),将NGT者按年龄分成5组,观察各年龄组的血糖水平,用稳态模式分析胰岛β细胞功能指数(HBCI),并对其进行统计学分析.结果 在NGT中60～69年龄组FPG值(5.17±0.48)mmol/L、糖化血红蛋白(HbA1c)(6.01±0.62)%较50～59年龄组FPG值(5.09±0.44)mmol/L、HbA1c值(5.95±0.66)%高(t值分别为2.06、2.48,P均<0.05).60～69年龄组FIG值较40～49年龄组FPG值(5.01±0.47)mmol/L高(t=2.26,P<0.01),50～59年龄组FPG值较40～49年龄组高(t=2.48,P<0.01),5组按年龄从小至大比较,空腹胰岛素(FINS)值变化无明显规律;60岁以上HBCI较60岁以下的HBCI值下降,差异有统计学意义(F值为33.75,P<0.01).结论 NGT人群随着年龄的增长,FPG、HbAlc可能增高.

Abstract：

Objective To compare the glucose levels and associated factors among the normal glucose tolerance subjects with different age.Methods Totally a community-based population of 2098 residences aged above 30 years Were tested with OGTT,and classified into normal glucose tolerance group(NGT),impaired glucose tolerance group(IGT),impaired fasting glucose group(IFG),both IGT and IFG group(ICT/IFC),anddiabetes group(DM) according to fasting and 2 hours glucose level(2 hPG).The subjects in NGT group were further divided into 5 groups according to different ages.The levels of blood glucose and HBCI in different groups and subgroups were measured and analyzed statistically. Results For patients in NGT,the FPG([5.17.±0.48]mmol/L vs.[5.09±0.44]mmol/L,P<0.05)and HbA1c([6.01±0.62]%vs.[5.95±0.66]%.P<0.05)in group aged 60-69 Were higher than that in group aged 50-59.The FPG in group aged 60-69 was also higher than those in group aged 40-49([5.17±0.48]mmol/L vs.[5.00±0.47]mmol/L,P<0.01),and the FPG in group aged 50-59 Was also higher than those in group aged 40-49([5.09±0.44]mmol/L vs..[5.00±0.47]mmol/L,P<0.01).There was no correlation between age and FINS,while a tendency of decreasing HBCI could be observed along with increasing of age(F=33.75,P<0.05).Conclusion In NGT subjects,the FPG and HbA1 C inereased along with age.     

糖调节受损患者血清超敏C反应蛋白和细胞间黏附分子-1水平的变化

目的检测空腹血糖调节受损(IFG)及糖耐量减低(IGT)人群空腹血清超敏C反应蛋白(hs-CRP)、细胞间黏附分子-1(ICAM-1)水平,探讨血清hs-CRP、ICAM-1与胰岛素抵抗(IR)之间的关系。方法选取健康对照组30例,IFG组30例,IGT组30例,IFG并IGT组30例,新发2型糖尿病组(T2DM)30例。对所有受试者空腹测血清hs-CRP、ICAM-1、血糖、甘油三酯、胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、空腹胰岛素等(FINS)项目,应用稳态模型评估法评价胰岛素抵抗指数(HOMA-IR)。结果各试验组的FINS、空腹血糖(FBG)、HOMA-IR均高于正常对照组,差异有显著性(P<0.05);IGT组、IFG并IGT组、T2DM组的CRP、ICAM-1高于正常对照组,差异有显著性(P<0.05);CRP、ICAM-1在IFG组与正常组之间无显著性差异(P>0.05)。T2DM组的FINS、FBG、HOMA-IR、CRP、ICAM-1高于IGT组,差异有显著性(P<0.05),IFG并IGT组与IGT组比较,上述指标均无显著性差异(P>0.05)。逐步多元回归分析显示,BMI、hs-CRP、ICAM-1是影响HOMA-IR的重要危险因素。结论 (1)T2DM组、糖调节受损人群(包括IFG、IGT、IFG并IGT)存在明显的胰岛素抵抗,CRP、ICAM-1、BMI是胰岛素抵抗的危险因素;(2)随着糖耐量受损的加重,血清hs-CRP、ICAM-1水平逐渐升高;(3)糖调节受损时期即可能存在内皮功能损伤,并出现大血管病变的一些病理生理改变(如急性时相蛋白CRP,ICAM-1)。     

不同糖代谢水平血清脂联素与胰岛素抵抗及血管舒张功能相关性研究

目的 研究不同糖代谢水平人群的血清脂联素与胰岛素抵抗、血管舒张功能的相关性.方法 体检人群中经口服葡萄糖耐量试验(OGTT)筛选出糖耐量正常(NGT)17例,空腹血糖调节受损(IFG)22例,糖耐量受损(IGT)23例、2型糖尿病(T2DM)21例,检测血清脂联素(APN)水平;用HOMA-IR和HOMA-β指数分别评价胰岛素抵抗指数、B细胞功能指数;采用高分辨率血管外超声检测血流介导的内皮依赖性血管舒张功能(EDVD)和硝酸甘油介导的内皮非依赖性血管舒张功能(EIVD).结果 在NGT,IFG,IGT,DM组,APN和EDVD水平依次降低;HOMA-IR逐渐增高.校正了年龄、性别、体质量指数、腰臀比后,APN与HOMA-IR呈负相关(r=-0.353,P<0.01),与EDVD和EIVD呈正相关(r分别为0.391,0.375,P<0.01),APN与HOMA-β无关(P>0.05);EDVD与HOMA-IR无关(P>0.05).多元逐步回归分析以APN为应变量,HOMA-IR进入方程(P<0.01);以EDVD为应变量,APN进入方程(P<0.05)HOMA-IR未进人方程.结论 T2DM 前期已经存在APN降低、胰岛素抵抗、血管内皮功能损害.APN与胰岛素抵抗负相关;与血管内皮功能正相关.APN与内皮依赖性血管舒张功能的关系独立于胰岛素抵抗.

Abstract：

Objective To study the correlation between serum adiponectin along with insulin resistanee and vascular dilation function in patients with different rates of glucose metabolism.Method A total of 83 patients aged 50-65 years,including 17 with normal glucose tolerance(NGT),22 with impaired fasting glucose (IFG),23 with impaired glucose tolerance(IGT)and 21 with diabetes(DM)were enrolled. Serum adiponectin was measured,and homeostasis model assessment for insulin resistance index (HOMA-IR)and B cell function index were used to evaluate the function of insulin secretion before and during oral glucose tolerance test(OGTr).The brachial artery responses to flow-mediated endothelium-dependent vascular dilation(EDVD)and nitroglycerin-mediated vascular dilation (EIVD) were evaluated by using the vascular ultrasound with high resolution.Results The serum adiponectin and EDVD decreased that the degrees of reduction from slightness to greatness were in turn from NGT,IFG,IGT to DM,whereas,the insulin resistance index (HOMA-IR) increased just in reverse order.Adiponectin was negatively associated with HOMA-IR(r=-0.353,P<0.01)but positively associated with EDVD and EIVD(rl=0.391,r2=0.375,P<0.01),and was not associated with HOMA-B.On the other hand,EDVD was not associated with HOMA-IR(P>0.05).In a multiple regression analysis with a stepwise manner to predict adiponectin concentration and EDVD.HOMA-IR was supposed to predict adiponectin concentration.Meanwhile APN but not HOMA-IR was used to predict EDVD(P<0.05).Condusions The decrease in serum adiponectin,endothelial dysfunction and insulin resistance can be observed in the early stage of impaired glucose metabolism. Serum adiponectin concentration appears to be associated with vascular function and insulin resistance.The association between serum adiponectin concentration and vascular function seems to be independence from its link with insulin resistance index.     

Differences in cardiovascular risk factors, insulin resistance, and insulin secretion in individuals with normal glucose tolerance and in subjects with impaired glucose regulation: the Telde Study

OBJECTIVE: To assess the cardiovascular risk profile, the degree of insulin resistance, and beta-cell secretion in a cohort of subjects with different categories of impaired glucose regulation (IGR): impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and combined IFG/IGT. RESEARCH DESIGN AND METHODS: We studied 902 nondiabetic subjects between 30 and 80 years of age, recruited from a cross-sectional population-based study in Telde, Gran Canaria Island, Spain. Categories of glucose tolerance were defined according to 2003 modified American Diabetes Association criteria. Risk factors for cardiovascular disease, the presence of the metabolic syndrome, and indirect measures of both insulin resistance and beta-cell function were analyzed. RESULTS: A total of 132 (14.6%) participants had isolated IFG, 59 (6.5%) isolated IGT, and 48 (5.3%) combined IFG/IGT. Groups with normal glucose tolerance (NGT) and combined IFG/IGT had, respectively, the most favorable and unfavorable levels of cardiovascular risk factors, metabolic syndrome rates, and measures of insulin resistance. Subjects with IFG and IGT showed an intermediate profile between NGT and IFG/IGT categories. We found no significant differences between IFG and IGT in cardiovascular risk factors, metabolic syndrome prevalence, or insulin resistance. The IFG group exhibited a more impaired insulin secretion than those with IGT or IFG/IGT. CONCLUSIONS: Individuals with IGR, especially those with IFG/IGT, have increased values of cardiovascular risk factors and higher indexes of insulin resistance. Groups with isolated IFG and isolated IGT present similar cardiovascular risk profiles. Subjects with IFG are characterized by more defective beta-cell function than other forms of IGR.