糖耐量低减患者红细胞胰岛素酶活性与胰岛素抵抗

目的:探讨糖耐量低减(IGT)患者的红细胞胰岛素酶活性(EIA)与胰岛素抵抗(IR)的关系。方法:用放射酶分析法检测50例IGT患者和20例正常对照的EIA及相关指标,并计算稳态模型胰岛素抵抗指数(HOMA-IR)以评价机体的胰岛素敏感性。结果:IGT患者的EIA、空腹血清胰岛素(FINS)和HOMA-IR指数显著高于正常对照(P<0.01),伴空腹血糖异常的IGT患者与空腹血糖正常的IGT患者相比,前者的EIA、FINS、HOMA-IR显著高于后者(P<0.01或0.05)。直线回归分析表明,IGT患者的EIA与FINS、HbA1c和HOMA-IR指数呈显著正相关(P<0.01或0.05)。结论:IGT患者的红细胞胰岛素降解速度显著高于正常,并与其IR的发生、发展有关。     

早发2型糖尿病家系一级亲属血清尿酸水平的横断面研究

目的研究尿酸在2型糖尿病发生发展中不同阶段的变化规律和相关因素。方法对200个早发2型糖尿病家系(至少一个患者在40岁前被诊断)的249例既往无糖耐量异常的2型糖尿病患者的一级亲属,进行口服75克葡萄糖耐量实验(OGTT),并检测糖化血红蛋白(HbA,c)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL—C)、低密度脂蛋白胆固醇(LDL—C)、尿酸(SUA)和肌酐(SCr),测量体质量指数(BMI)和腰臀比(WHR);用稳态模型胰岛素抵抗指数(HOMA—IR)评估胰岛素抵抗,胰岛8细胞功能指数(HOMA-8)评估8细胞胰岛素基础分泌,采用OGTT中空腹和30分钟胰岛素血糖差值的比值(△130／△G30)评价胰岛素早期分泌,用△130／△G30／HOMAIR评估处置指数(desposition index,DI)。结果①总共50例新诊断糖尿病(DM),58例被诊断为空腹血糖受损(IFG)和(或)糖耐量减低(IGT),统称糖调节受损(IGR),141例OGTT和HbA1c均正常(NGT);②DM、IGR和NGT组间尿酸差异无统计学意义,但DM组HOMA-β、△130／△G30、DI显著低于IGR和NGT组,HOMAIR高于IGR和NGT组;DM和IGR组的BMI、WHR、OGTT2小时胰岛素显著高于NGT组;DM组的HDL—c显著低于而TG显著高于NGT和IGR组;③将141例NGT者按HbA1c中位数(5．4％)分组后比较发现,高HbA1c组与低HbA1c组的尿酸水平差异无统计学意义,但高HbA1c组HOMAIR、空腹胰岛素水平、BMI已经显著高于低HbA1c组;④在NGT组,调整年龄、BMI、血压、TG后,男性的尿酸水平仍高于女性;⑤在所有的个体中,Pearson相关分析发现,不论男性还是女性,血尿酸与BMI、WHR、甘油三酯、空腹胰岛素、HOMAIR、和Scr正相关;逐步多元回归分析,发现SCr、BMI、性别、TG是影响血清尿酸的独立因素。结论本研究没有观察到血尿酸水平在2型糖尿病发生的不同阶段显著性变化,尿酸变化并不是2型糖尿病前期的病理生理改变,它的改变可能发生在体质量增加、胰岛素分泌和敏感性下降后,Scr、性别、BMI、TG是影响尿酸水平的独立因素。     

马来酸罗格列酮对2型糖尿病患者颈动脉内膜中层厚度的影响

目的观察在2型糖尿病(T2DM)的患者中应用马来酸罗格列酮治疗对其颈总动脉内膜中层厚度(IMT)的影响。方法T2DM患者(T2DM组)与糖耐量正常者(NGT组)各30例分别检测空腹血糖(FPG)、血胰岛素(FIns)、糖基化血红蛋白(HbA1c),计算胰岛素抵抗指数(HOMA-IR),同时测定超敏C反应蛋白(hsCRP),并应用超声仪测定IMT,然后T2DM组接受马来酸罗格列酮治疗12个月后再次检测上述指标,比较各指标的变化。结果T2DM组的FPG、FIns、HbA1c、HOMA-IR、hsCRP和IMT均显著高于NGT组(P<0.05或P<0.01);马来酸罗格列酮治疗后IGT组的上述指标与治疗前相比均显著下降(P<0.05或P<0.01)。结论马来酸罗格列酮治疗可改善T2DM患者胰岛素抵抗状态,降低炎症反应,并可能缓解动脉粥样硬化的发生和发展。     

吡咯列酮对糖耐量低减并高胰岛素血症患者糖代谢及部分炎症因子的影响

目的:探讨吡咯列酮对合并高胰岛素血症的糖耐量减低(IGT)患者血糖(PG)、血胰岛素(Ins)、胰岛素抵抗及炎症因子白细胞介素-6(IL-6)、高敏C反应蛋白(hs-CRP)的影响。方法:60例IGT并高胰岛素血症患者随机分为两组,各30例,分别予盐酸吡咯列酮及安慰剂干预治疗15周,测体质指数(BMI)、空腹及负荷后PG、Ins、糖化血红蛋白(HbA1c)、胰岛素敏感性指数(ISI)、IL-6、hs-CRP等。结果:安慰剂组用药前后各项指标差异无统计学意义(P>0.05);吡咯列酮组空腹血糖(FBG)、负荷后2h血糖(2hPBG)、HbA1c、空腹胰岛素(Fins)、负荷后2h胰岛素(2hIns)、IL-6、hs-CRP均明显下降,ISI明显回上升(P<0.05或P<0.01),两组间比较差异有统计学意义(P<0.05或P<0.01)。结论:吡咯列酮可改善IGT并高胰岛素患者的糖代谢状态,减轻高胰岛素血症,改善胰岛素分泌,同时可降低IL-6、hs-CRP水平,减轻炎症反应。     

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     

不同糖耐量的老年高血压患者颈动脉粥样硬化与胰岛素抵抗及炎性因子的相关性

目的探讨不同糖耐量老年高血压患者颈动脉粥样硬化与胰岛素抵抗(IR)及炎性因子的相关性。方法 94例老年高血压患者进行葡萄糖耐量实验(OGTT),根据OGTT结果分为糖耐量正常组(NGT组)30例、糖耐量异常组(IGT组)32例、2型糖尿病组(DM组)32例,同时选取30例健康体检者为对照组。4组患者均行超声检查颈动脉内膜-中层厚度(IMT),测定空腹血糖(FPG)、空腹胰岛素(FIns)、血脂、hs-CRP及TNF-α等指标,采用自我平衡模型分析法(HOMA)计算胰岛素抵抗指数(HOMA-IR)。结果 HOMA-IR、hs-CRP、TNF-α及IMT等指标DM组明显高于其余3组,IGT组明显高于NGT组及对照组,NGT组明显高于对照组(P<0.01),相关性分析显示IMT与HOMA-IR、hs-CRP、TNF-α水平呈正相关(r分别为0.406、0.420、0.396,P<0.05)。结论在老年高血压患者中存在IR和炎性反应,老年高血压患者的HOMA-IR、hs-CRP、TNF-α与颈动脉IMT密切相关。     

血脂紊乱对糖尿病患者胰岛素抵抗及胰岛功能的影响

目的 探讨血脂紊乱对糖尿病患者胰岛素抵抗及胰岛功能的影响。方法 选取2021年2月至2023年2月郑州大学第一附属医院收治的糖尿病患者91例为研究对象，根据患者血脂情况分为血脂正常组(n=31)与血脂异常组(n=60)。血脂异常组根据血脂异常情况分为高胆固醇组(n=21)、高三酰甘油组(n=21)以及两者同时存在的混合组(n=18)。比较各组血糖[空腹血糖(FBG)、糖化血红蛋白水平(HbA1c)、负荷后某时点血糖(G120)]水平；比较各组胰岛素抵抗情况[空腹胰岛素(FINS)、胰岛素抵抗水平(HOMA-IR)、胰岛素敏感性指数(HOMA-IS)及空腹C肽(FC)]和胰岛功能[胰岛β细胞功能(HOMA-β)、早期胰岛素分泌指数(EISI)、负荷后某时点胰岛素(I30)、胰岛素曲线下面积(AUCI)、血糖曲线下面积(AUCG)及调整胰岛素抵抗后的早期分泌指数(REISI)]。结果 各组FBG、HbA1c及G120比较差异未见统计学意义(P>0.05)。高三酰甘油组及混合组FC、HOMA-IR高于血脂正常组及高胆固醇组(P<0.05),各组HOMA-IS比较差异未见统计学意义...     

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。     

2型糖尿病患者胰岛素抵抗与血清游离脂肪酸浓度的关系

目的探讨2型糖尿病(T2DM)患者空腹与餐后2 h游离脂肪酸(FFA)浓度和胰岛素抵抗的关系。方法测定100例T2DM患者(根据亚洲糖尿病论坛的推荐分为控制良好和控制不良2组)及50名正常对照者的糖化血红蛋白(HbA1c)、空腹胰岛素(FINS)、空腹血糖(FPG)、餐后2 h血糖(2 h PG)、空腹FFA及餐后2 hFFA。以稳态模式评估胰岛素抵抗指数(HOMA-IR)。结果与对照组比较,T2DM组的FPG、2 h PG、FFA、2 h FFA、HbA1c、HOMA-IR均明显增高(P<0.01)。T2DM控制不良组各项指标均高于控制良好组(P<0.05),FFA、2 h FFA与HOMA-IR、HbA1c、FPG、2 h PG均呈明显的正相关(r分别为0.910、0.876,0.851、0.759,0.908、0.746,0.769、0.674,P<0.01)。结论 T2DM患者体内FFA浓度的增高与胰岛素抵抗存在明显相关性,与T2DM的发病机制有密切关系。     

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.     

Natural History of Insulin Sensitivity and Insulin Secretion in the Progression From Normal Glucose Tolerance to Impaired Fasting Glycemia and Impaired Glucose Tolerance: The Inter99 Study

OBJECTIVE—The aim of this study was to describe the natural history of insulin secretion and insulin sensitivity in the development of isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), and combined IFG/IGT.RESEARCH DESIGN AND METHODS—Baseline and 5-year follow-up data from the Inter99 study were used. Individuals with normal glucose tolerance (NGT) at baseline and i-IFG, i-IGT, combined IFG/IGT, or NGT at the 5-year follow-up were examined with an oral glucose tolerance test (n = 3,145). Insulin sensitivity index (ISI), homeostasis model assessment of insulin sensitivity (HOMA-IS), early-phase insulin release (EPIR), and insulin secretion relative to insulin action (disposition index) were estimated.RESULTS—Five years before the pre-diabetes diagnoses (i-IFG, i-IGT, and IFG/IGT), ISI, HOMA-IS, EPIR, and disposition index were lower than in individuals who maintained NGT. During the 5-year follow-up, individuals developing i-IFG experienced a significant decline only in HOMA-IS, whereas individuals developing i-IGT experienced significant declines in ISI, EPIR, and disposition index. Individuals with IFG/IGT exhibited pronounced declines in ISI, HOMA-IS, EPIR, and disposition index during the 5-year follow-up.CONCLUSIONS—A stationary reduced insulin secretion followed by a decline in primarily hepatic insulin sensitivity characterizes the transition from NGT to i-IFG. In contrast, low whole-body insulin sensitivity with a secondary lack of β-cell compensation is associated with the development of i-IGT. Thereby, i-IFG and i-IGT appear to result from different underlying mechanisms, which may have implications for the prevention and treatment of the diabetes that succeeds them.During the past few years, it has been established that the pre-diabetic conditions of isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), and combined fasting and postchallenge hyperglycemia (IFG/IGT) represent distinct pathways to diabetes. These pre-diabetic states are characterized by different degrees of insulin sensitivity, insulin secretion, and hepatic glucose output as well as secretion of glucagon and incretin hormones (1–8). Nevertheless, the primary abnormalities inherent in the different pre-diabetic conditions are still unknown.Randomized trials have shown beneficial effects of lifestyle intervention on diabetes risk in individuals with i-IGT and IFG/IGT (9,10), but whether lifestyle interventions have the same preventive effects in individuals with i-IFG is not known. Indeed, a more profound insight into the pathogenesis of the disease is needed to optimize prevention and treatment of type 2 diabetes. In particular, focus on the initial defects responsible for hyperglycemia in the fasting and postprandial states is essential for interrupting the progression from normal to abnormal glucose metabolism.Most previous studies have examined the pathophysiology of pre-diabetes in cross-sectional settings without knowing the time of onset of glycemic abnormalities. However, the observed abnormalities in pre-diabetes may be related to traits already apparent in the normoglycemic state. Prospective studies are therefore needed to clarify whether this is the case or whether the metabolic abnormalities associated with i-IFG, i-IGT, and IFG/IGT develop simultaneously with the increases in fasting and/or postchallenge plasma glucose levels.The aim of this study was to describe the natural history of insulin sensitivity and insulin secretion during the progression from normal glucose tolerance (NGT) to the pre-diabetic states of i-IFG, i-IGT, and combined IFG/IGT.     

老年高血压患者血糖与颈动脉内膜中层厚度及动脉弹性的相关性

摘要 目的 探讨老年高血压患者血糖变化对颈动脉内膜中层厚度和动脉弹性的影响是否有叠加作用。方法 82例老年高血压患者根据糖耐量试验分成糖耐量正常组（NGT组）、空腹血糖受损组（IFG组）、糖耐量减低组（IGT组）和糖尿病组（DM组），26例健康体检者作为对照组（NC组）。通过超声检测颈动脉内膜中层厚度（IMT），用动脉硬化检测仪测量颈-股动脉脉搏波的传导速度（PWV）。结果 老年高血压患者IMT、PWV显著高于健康对照者。由NGT组到IFG组、IGT组、DM组，IMT、PWV逐渐增加，IFG组IGT组间无显著性差异。在无血糖紊乱的情况下，脉压和年龄是影响IMT、PWV的主要因素。当存在糖代谢异常时，糖化血红蛋白、餐后2小时血糖可影响IMT、PWV。结论 老年高血压患者，IMT增厚，动脉弹性降低。血糖代谢异常加重了老年高血压患者IMT增厚及动脉弹性的减退，使其心血管并发病的风险加大。     

Factors responsible for development from normal glucose tolerance to isolated postchallenge hyperglycemia

OBJECTIVE: Isolated postchallenge hyperglycemia (IPH), defined as fasting plasma glucose (FPG) level <7.0 mmol/l and 2-h plasma glucose (PG) level >/=11.1 mmol/l, is a subtype of early-stage diabetes. This study evaluates the metabolic profiles of insulin secretion and insulin sensitivity in IPH to clarify the factors responsible for development of this form of type 2 diabetes. RESEARCH DESIGN AND METHODS: We conducted cross-sectional analysis of 231 Japanese men aged 20-70 years. The subjects were classified into the following three groups, based on the results of a 75-g oral glucose tolerance test (OGTT): 1) normal glucose tolerance (NGT), defined as FPG level <6.1 mmol/l and 2-h PG level <7.8 mmol/l (n = 89); 2) impaired glucose tolerance (IGT), defined as FPG level <7.0 mmol/l and 2-h PG level of 7.8-11.1 mmol/l (n = 94); and 3) IPH (n = 48). We compared the three groups for insulin secretion (insulinogenic index) and insulin sensitivity (index of insulin resistance using homeostasis model assessment [HOMA-IR]). RESULTS: The insulinogenic index in IPH was the lowest of the three groups (P < 0.001 versus NGT). The HOMA-IR in the IGT and IPH groups were significantly higher than in the NGT group (P < 0.001), but both were similar. By linear regression analysis, the insulinogenic index rather than fasting insulin or HOMA-IR was the more significant factor in the 2-h PG level in IGT and IPH. CONCLUSIONS: Subjects with IPH exhibited distinctly impaired early-phase insulin secretion and only mild insulin resistance, indicating that reduced insulin secretion is the primary determinant of deterioration from NGT to IGT and IPH in development of type 2 diabetes in these subjects.     

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.     

高频超声评价2型糖尿病颈动脉内膜-中层厚度与心血管病变的相关性

目的探讨高频彩色多普勒超声在评价2型糖尿病患者颈动脉内膜-中层厚度(IMT)与心血管病变相关性中的应用价值。方法对31例健康人(组1)及54例2型糖尿病患者,分为无高血压病、无冠心病者(组2,32例),合并高血压组(组3,12例),合并冠心病组(组4,10例),采用高频超声分别测定颈总动脉主干、壶腹部、颈内动脉IMT最大值(IMTmax)及平均值(IMTmean,为3次测量的均值),以颈总动脉后壁IMT平均值作为评定指标。在禁食12～14h后采各组静脉血,测定空腹血糖(FBG)、胰岛素(Fin)、总胆固醇(TCh)、甘油三脂(TG)、高密度脂蛋白-胆固醇(HDL-C)、糖化血红蛋白(GHb),并计算体重指数(BMI)、腰臀围比值(WHR),测量收缩压(SDP)及舒张压(DBP),并对各组检测结果行统计学处理分析。结果糖尿病患者颈总动脉IMT大于正常对照组(P<0.05),合并冠心病、高血压组较非合并组有更高IMT值及动脉硬化斑块数(P<0.05)。多元回归分析结果显示,年龄及DBP是2型糖尿病患者IMT值的独立危险因素。结论高频彩色多普勒超声可有效测量糖尿病患者颈总动脉IMT值或斑块数,尤其是在2型糖尿病合并心血管病变时应用价值更大。     

The relationship between left ventricular mass index and insulin sensitivity, postprandial glycaemia, and fasting serum triglyceride and adiponection levels in patients with type 2 diabetes

The relationship between left ventricular mass index (LVMI) and insulin sensitivity, postprandial glycaemia, fasting serum triglyceride and adiponectin was investigated in 70 patients with type 2 diabetes. Serum fasting insulin, C-peptide, high-sensitivity C-reactive protein (hs-CRP), glycated haemoglobin (HbA1c), postprandial glycaemia, lipids and fasting serum adiponectin levels were measured. Ventricular hypertrophy was assessed at rest by electrocardiography and echocardiography. Insulin sensitivity was assessed using the homeostasis model assessment index (HOMA-IR). LVMI was assessed using the Devereux formula. Study patients had lower than normal HOMA-IR, and higher than normal serum fasting insulin levels and LVMI, and tended to have reduced insulin sensitivity. Pearson's correlation coefficient showed a statistically significant correlation between fasting serum adiponectin and LVMI, fasting serum insulin, HOMA-IR, HbA1c, serum postprandial glucose and hs-CRP. There were no statistically significant correlations between LVMI and serum hs-CRP or HOMA-IR. The results indicate the importance of fasting serum adiponectin in the development of cardiovascular complications, such as increased LVMI.     

空腹血清游离脂肪酸与2型糖尿病的关系

目的 2型糖尿病(T2DM)患者血清游离脂肪酸(FFA)水平的变化及与糖代谢、胰岛素抵抗各指标间的相关性,并探讨影响T2DM的危险因素。方法通过口服糖耐量试验(OGTT)筛选105例未经药物治疗的T2DM患者和66名健康人(正常对照组),分别测定其血浆葡萄糖(PG)和胰岛素(Ins)水平,计算胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-IS),同时检测空腹血清FFA。对血清FFA浓度与性别、年龄、体重、体重指数(BMI)、0～3 h PG和Ins以及HOMA-IR、HOMA-IS进行相关性分析。以T2DM是否发病为因变量Y(T2DM组=1,正常对照组=0),性别、年龄、体重、BMI、HOMA-IR、HOMA-IS和FFA为自变量,做Logistic回归分析。结果 T2DM组HOMA-IR、HOMA-IS和血清FFA水平与正常对照组比较差异均有统计学意义(P<0.01、P<0.001)。相关分析发现,空腹血清FFA与0 h PG、0.5 h PG、1 h PG、2 h PG、3 h PG、3 h Ins、HOMA-IR呈弱正相关(r分别为0.340、0.281、0.282、0.307、0.302、0.193、0.225,P均<0.05)。Logistic回归分析显示血清FFA是T2DM的重要风险因素[OR=14.05,95%可信区间(CI):1.87～105.55]。结论血清FFA水平升高可能影响机体糖动态平衡,与胰岛素抵抗和T2DM发病密切相关。