2型糖尿病合并心血管病患者B型尿钠肽水平变化及与超敏C反应蛋白和脂蛋白(a)的关系

目的:分析2型糖尿病(T2DM)合并心血管病患者血浆B型尿钠肽(BNP)水平变化及与血清超敏C反应蛋白(hs-CRP)和脂蛋白(a)[Lp(a)]浓度的关系。方法:将49例T2DM患者分为单纯T2DM组(n=28)和T2DM合并心血管病组(n=21),同时选择30例健康体检者作为健康对照组。采用化学免疫发光法检测血浆BNP,采用透射比浊法检测血清hs-CRP,采用胶乳比浊法检测Lp(a);比较各组以上指标水平变化,并分析T2DM合并心血管病患者BNP水平与hs-CRP和LP(a)浓度的相关性。结果:T2DM合并心血管病组BNP、hs-CRP及Lp(a)水平均显著高于健康对照组和单纯T2DM组(P<0.05);单纯T2DM组BNP和hs-CRP的检测结果显著高于健康对照组(P<0.05),而Lp(a)在此两组间无显著性差异(P>0.05)。T2DM合并心血管病组血浆BNP与血清hs-CRP水平呈显著正相关(r=0.467,P<0.05),而与Lp(a)无明显相关性;hs-CRP与Lp(a)亦无明显相关性。结论:血浆BNP水平显著升高可提示T2DM患者合并心血管病变。     

吡格列酮对2型糖尿病患者血浆内皮素和一氧化氮水平的影响

目的:探讨吡格列酮对2型糖尿病(T2DM)患者血浆内皮素(ET)、一氧化氮(NO)的影响。方法:70名T2DM患者,随机双盲分为安慰剂组(A组,35例)和吡格列酮组(B组,35例),治疗3个月后,检测两组患者服药前后空腹血糖(FBG)、空腹胰岛素(FINS)、糖基化血红蛋白(HbA1C)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、ET和NO,并计算胰岛素敏感指数(ISI)。结果:治疗后吡格列酮组FBG、FINS、HbA1C、TG、ET明显下降(P<0.01),HDL-C、ISI、NO显著升高(P<0.01),ET与FINS呈正相关(r=0.478,P<0.01),与ISI呈负相关(r=-0.306,P<0.01),NO与FINS呈负相关(r=-0.371,P<0.01),与ISI呈正相关(r=0.447,P<0.01);安慰剂组各参数于治疗前后无显著性差异。结论:吡格列酮能够显著降低T2DM患者的ET水平,升高NO水平。     

2型糖尿病患者C反应蛋白、脂联素和瘦素水平与胰岛素抵抗的相关性

目的探讨C反应蛋白(CRP)、脂联素(APN)、瘦素(Leptin)水平、胰岛素抵抗指数(HOMA-IR)与2型糖尿病(T2DM)病变易患因素的关系。方法用RIA法测定2型糖尿病患者血浆leptin和胰岛素(FINS),用ELSIA法测定血清ANP,用全自动生化分析仪常规测定血清CRP、空腹血糖(FPG),计算胰岛素抵抗指数(HOMA-IR,FPG×FINS/22.5),以正常健康体检者为对照组,进行对比分析。结果 CRP、leptin、HOMA-IR在2型糖尿病组显著高于对照组(P<0.01),ANP显著低于对照组(P<0.01);线性相关显示2型糖尿病HOMA-IR与CRP(r=0.36,P<0.05)、leptin(r=0.39,P<0.05)呈正相关,2型糖尿病HOMA-IR与APN(r=-0.32,P<0.05)呈负相关。结论低APN和高CRP、leptin血症可能是糖尿病的发病因子,它们的代谢紊乱与胰岛素抵抗有密切关系。     

不同糖耐量水平患者胰岛素抵抗与皮质醇、醛固酮相关研究

目的 探讨不同糖耐量水平患者的皮质醇、醛固酮、胰岛素抗体与胰岛素抵抗水平的关系.方法 选择115例糖耐量增高的患者,根据糖尿病诊断标准分为糖尿病(T2DM)组(39例)、糖尿病前期(PD)组(35例)、血糖受损(IGR)组(41例)作为研究对象.所有受试对象均在空腹条件下,测定体重指数(BMI),口服75g葡萄糖耐量试验(OGTT)和胰岛素释放实验,以稳态模型公式计算胰岛素抵抗指数(HOMA-IR),同时进行空腹血浆皮质醇、血浆醛固酮以及胰岛素抗体检测,研究胰岛素抵抗指数与皮质醇、醛固酮以及胰岛素抗体的关系.结果 T2DM组、PD组和IGR组HOMA-IR同正常糖耐量组(NGT)比较,差异有显著性(P＜0.01);血浆皮质醇(COR)与HOMA-IR呈正相关(r=0.14,P＜0.05),胰岛素抗体和血浆醛固酮与HOMA-IR无相关性.结论 糖耐量增高的患者存在胰岛素抵抗,伴有肥胖者皮质醇明显增高,皮质醇与胰岛素抵抗具有相关性.     

2型糖尿病患者血清25-羟基维生素D水平分析

目的:分析2型糖尿病(T2DM)患者血清25-羟基维生素D(25-OH VitD)水平及其与胰岛素抵抗、胰岛β细胞功能的关系。方法:检测328例T2DM患者(T2DM组)和50例常规体检正常者(正常对照组)血清25-OH VitD、空腹胰岛素(FINS)、C-肽(C-p)、空腹血糖(FPG)、糖化血红蛋白(HbA1c)水平,计算稳态模型-胰岛素抵抗指数(HOMA-IR)和稳态模型-胰岛β细胞功能指数(HOMA-β),并作统计分析。结果:正常对照组男性与女性血清25-OH VitD水平差异无统计学意义(P0.05),T2DM组男性与女性血清25-OH VitD水平差异亦无统计学意义(P0.05)。T2DM组男性、女性血清25-OH VitD和HOMA-β水平分别低于正常对照组男性、女性水平(P0.05)。T2DM患者组男性、女性的FINS、FPG、HbA1c、HOMA-IR水平分别高于正常对照组男性、女性水平(P0.05)。T2DM患者血清25-OH VitD水平与HOMA-β呈正相关(r=0.306,P0.05);与HOMA-IR呈负相关(r=-0.173,P0.05)。结论:T2DM患者血清25-OH VitD水平降低与胰岛素抵抗增加及胰岛β细胞功能降低有关。     

脂质灌注对大鼠血浆抵抗素和ghrelin的影响*

目的：探讨脂质灌注对大鼠血浆抵抗素和ghrelin的影响。 方法： 采用正糖钳夹技术，在钳夹前后分别测定生理盐水对照组和脂质灌注组血浆抵抗素和ghrelin浓度，并用［3H］-葡萄糖作为示踪剂测定外周组织和肝糖的代谢。 结果： 脂质灌注组大鼠血浆游离脂肪酸（FFA）明显增加（P<0.01），葡萄糖输注率（GIR）明显降低（P<0.01）。对照组肝糖产率（HGP）明显被抑制（88%）。脂质输注组胰岛素对HGP的抑制作用明显减弱。在钳夹期间，脂质组与对照组比葡萄糖清除率（GRd）轻度降低。在正糖钳夹术结束时，对照组血浆ghrelin水平与钳夹前相比明显降低(P<0.05)。4 h的脂质灌注也引起了血浆ghrelin浓度的明显下降(P<0.05)，但是在钳夹结束时和对照组比没有明显差异。相关性分析表明空腹血浆ghrelin水平与空腹胰岛素和血糖呈明显负相关（r=-0.52和r=-0.61, P<0.05）。脂质灌注后大鼠血浆抵抗素水平较灌注前和对照组明显升高（P<0.01），空腹血浆抵抗素浓度与空腹FFA（r=0.68, P<0.01）、血糖（r=0.66, P<0.01）呈明显正相关。 结论： 脂质灌注诱导了肝脏和外周的胰岛素抵抗，抵抗素在胰岛素抵抗的形成中可能具有重要作用。高胰岛素血症，而不是游离脂肪酸，降低了大鼠循环ghrelin水平。     

老年人血浆游离脂肪酸浓度、血糖水平与肥胖的关系

目的 研究老年人血浆游离脂肪酸(FFA)浓度、空腹血糖水平与超重及肥胖的关系.方法 对154例年龄≥60岁的志愿者,依据体重指数(BMI)分为肥胖组(41名)、超重组(39名)和正常体重组(74名),抽取空腹静脉血,检测血糖、胰岛素、血游离脂肪酸.结果 肥胖组、超重组FFA均显著高于正常体重组(P＜0.01).肥胖组空腹血糖高于超重组、正常体重组(P＜0.01),超重组空腹血糖高于正常体重组(P＜0.01).正常体重组、超重组FFA均与空腹血糖正相关(r:0.588、0.680,P均＜0.05),与胰岛素敏感指数(ISI)负相关(r=:-0.387、-0.354,P均＜0.05);肥胖组FFA与空腹血糖正相关(r =0.340,P＜0.05),与胰岛素敏感指数(ISI)无相关(P＞0.05).在以FFA为应变量的多元回归方程中,空腹血糖、ISI进入方程(R2 =0.451,P＜0.01).结论 血游离脂肪酸浓度与血糖水平相互影响,并与老年超重、肥胖密切相关.     

肥胖女童血清apelin、chemerin水平及其与胰岛素抵抗的关系

目的: 探讨肥胖女童血清apelin、chemerin水平及其与胰岛素抵抗的关系。方法: 35名女童参加本研究,肥胖组20人,年龄(9.73±2.08)岁,对照组15人,年龄(10.61±1.93)岁,两组年龄无显著差异(P>0.05)。采用ELISA法检测血清apelin和chemerin水平。空腹血脂和空腹血糖通过生化检测测定。空腹胰岛素通过化学发光法检测。计算每个个体的体重指数(BMI)、体重指数Z积分(BMI-SDS)及胰岛素抵抗指数(HOMA-IR)。结果: 肥胖组和对照组BMI存在明显差异(24.02±3.90 vs 16.46±1.93,P<0.01)。与对照组相比,肥胖组患者具有较高的甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、空腹胰岛素(FINS)和HOMA-IR水平(均P<0.05)。肥胖女童血清apelin水平较对照组高 ,血清chemerin水平明显较对照组高 。对所有参与研究者相关因素分析发现,血清apelin水平与BMI-SDS(r=0.356, P<0.05)、TG (r=0.548, P<0.01)、FINS(r=0.54 , P<0.01)及HOMA-IR(r= 0.55, P<0.01)呈正相关。血清chemerin水平与年龄呈负相关(r=-0.362,P<0.05),与BMI-SDS (r= 0.315, P< 0.01)、TG (r= 0.28, P< 0.05) 、FINS (r=0.38, P< 0.01)及HOMA-IR (r= 0.41, P< 0.01) 均呈正相关。血清apelin与chemerin水平呈正相关(r=0.34, P<0.05)。结论: 女童血清apelin、chemerin水平与胰岛素抵抗密切相关,apelin和chemerin可能参与儿童肥胖的代谢改变。     

瘦素、抵抗素、2型糖尿病间的相关性研究

目的：研究血浆瘦素与抵抗素、体重指数、腰围、腰臀比、血脂、胰岛素敏感性指数等的关系。方法：对43例新诊断2型糖尿病患者及37例糖耐量正常者，测定空腹血浆瘦素、胰岛素、血糖、血脂及抵抗素浓度。结果：相关分析显示性别、体重指数（BMI）、腰围、腰臀比、胰岛素与瘦素呈显著正相关（r分别为0.623,0.534，0.516，0.302，0.354，均P<0.01），IAI与瘦素呈显著负相关(r=-0.373,P<0.01),甘油三酯、胆固醇空腹血糖与瘦素无明显相关。瘦素与抵抗素无相关性（r=0.101,P>0.05）结论：空腹血浆瘦素水平与肥胖程度、胰岛素抵抗呈显著正相关，与抵抗素无关。瘦素可能与2型糖尿病的发病有关。     

糖尿病视网膜病变患者血浆Hcy、CEC和ET水平的检测分析

目的:分析糖尿病视网膜病变患者血浆同型半胱氨酸(Hcy)、外周血循环内皮细胞(CEC)和血浆内皮素(ET)水平及其相互关系。方法:将80例2型糖尿病(T2DM)患者分为2组:无糖尿病视网膜病变(NDR)组50例,糖尿病视网膜病变(DR)组30例,以我院健康体检正常者30例为对照(NC)组。分别测定Hcy、CEC、ET水平。结果:T2DM患者Hcy、CEC和ET水平均明显高于对照组(P<0.01);DR组Hcy、CEC、ET明显高于NDR组(P<0.01)。DR组血浆CEC计数和ET浓度呈正相关(r=0.839,P<0.05),Hcy浓度与CEC计数呈正相关(r=0.615,P<0.05),Hcy与ET浓度亦呈正相关(r=0.642,P<0.05)。结论:T2DM患者血浆Hcy、CEC、ET水平升高与DR有密切关系,血浆Hcy升高及内皮损伤可能在糖尿病患者视网膜病变的发生和发展中起重要作用。     

子痫前期患者孕中期血清脂联素水平及胰岛素抵抗的变化及意义

目的测定子痫前期（preeclampsia,PE）孕妇孕中期血清脂联素及胰岛素抵抗的变化并探讨其意义。方法随机选择2009年7月至2010年7月在青岛大学医学院第二附属医院门诊检查的孕妇300名,进行前瞻性研究分析,根据妊娠结局,发展为子痫前期共31人纳入研究组（PE,n=31）,同时选取30名正常孕妇作为对照组。于24～28孕周时,采用放射免疫吸附法测定血清脂联素（adiponectin,APN）、胰岛素（Fastig insulin,Fins）,并测定空腹血糖（fasting blood sugar,FBG）及其他临床指标,稳定模型的胰岛素抵抗指数（homeostatic model assessment-insulin resistance,HOMA-IR）用（Fins×FBG）/22.5来表示。并进行相关分析。结果①子痫前期组孕妇平均动脉压（mean arterial blood pressure,MABP）与对照组比较明显升高,有统计学意义（P〈0.01）。②研究组与对照组比较,血清脂联素水平明显降低,有统计学差异（P〈0.01）。血清胰岛素及HOMA-IR明显升高,有统计学差异（P均〈0.01）。FBG两组比较无统计学差异（P〉0.05）。③研究组孕妇血清脂联素与胰岛素、HOMA-IR及MABP呈负相关（r=-0.87,r=-0.44,r=-0.51,P均〈0.01）,与BMI无相关关系（r=-0.26,P〉0.05）。研究组孕妇HOMA-IR与胰岛素、MABP呈正相关（r=0.42,r=0.77,P均〈0.01）,与BMI无相关关系（r=-0.04,P〉0.05）。结论孕中期低脂联素水平及高胰岛素抵抗与子痫前期的发生有关。     

多囊卵巢综合征患者血清IGF-1水平与胰岛素抵抗

目的探讨血清胰岛素样生长因子1(IGF-1)、胰岛素敏感指数(ISI)与多囊卵巢综合征(PCOS)的关系。方法采集90例PCOS患者和41例正常对照组血清,应用电化学发光法检测胰岛素水平,葡萄糖氧化酶终点法检测空腹葡萄糖(FPG)水平,酶联免疫吸附试验(ELISA)检测IGF-1水平。结果 1.PCOS患者FPG、血清胰岛素、IGF-1水平明显高于正常对照组(t=16.72,2.24,4.51;P<0.01),且均与患者是否肥胖高度相关(t=5.08,2.07,3.30;P<0.01);2.PCOS患者胰岛素敏感性明显低于对照组,差别有显著性意义(t=3.12,P<0.05);3.PCOS患者血清IGF-1的含量与胰岛素敏感指数呈显著负相关,差别有显著性意义(r=-0.57,P<0.05);对照组血清IGF-1含量与胰岛素敏感指数无明显相关性(r=0.14,P>0.05)。结论多囊卵巢综合征患者存在不同程度的胰岛素抵抗(IR),IGF-1水平增高与PCOS患者发生IR有关,IGF-1可能与PCOS发生、发展有一定的内在联系并起协同作用。     

脂蛋白(a)基因单核苷酸多态性与钙化性主动脉瓣疾病及冠心病的关系

目的 探讨脂蛋白(a)[Lp(a)]基因单核苷酸多态性(SNP)与钙化性主动脉瓣膜疾病(CAVD)、冠心病(CHD)的相关性。方法 前瞻性研究。纳入2018年1-12月天津市胸科医院心内科CAVD或CHD住院患者248例,根据心脏超声多普勒、冠状动脉造影或冠状动脉CT检查结果分为两组:CAVD组101例、CHD组147例;同时选取2018年3-12月天津市胸科医院体检中心排除CAVD或CHD的171位健康体检者为对照组。检测各组Lp(a)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、载脂蛋白A(ApoA)、载脂蛋白B(ApoB)等生化指标,采用SNaPshot SNP分型技术对Lp(a)基因rs7770628、rs6415084、rs10455872三个位点进行基因分型;采用二元logistic回归分析不同基因型及Lp(a)水平对钙化性主动脉瓣疾病及冠心病发病的影响,采用线性回归分析不同基因型及ApoB水平对Lp(a)水平的影响。结果 三组间比较,患者BMI和饮酒史差异均无统计学意义(P值均＞0.05),性别、年龄、吸烟史、糖尿病史、高血压病史差异均有统计学意义(P值均＜0.05)。Lp(a) 检测值在对照组、CAVD组、CHD组分别为23.6(9.4,48.6)、37.2(16.5,79.6)、46.7(21.5,104.6)nmol/L,三组间比较差异有统计学意义(H=13.337,P<0.01);LDL值各组分别为(2.74±0.80)、(3.07±0.81)、(3.14±1.18)mmol/L,三组间差异有统计学意义(F=3.662,P<0.05);HDL值各组分别为(1.24±0.93)、(1.18±0.30)、(1.09±0.33 )mmol/L,三组间比较差异有统计学意义(F=4.281,P<0.05);ApoA值各组分别为(1.42±0.25)、(1.30±0.26)、(1.26±0.26) g/L,三组间比较差异有统计学意义(F=7.339,P<0.01);ApoB检测值各组分别为0.97(0.82, 1.10)、1.04(0.87, 1.26)、1.12(0.88, 1.31)g/L,三组间比较差异有统计学意义(H=3.948,P<0.05)。Lp(a)基因rs7770628位点对照组、CAVD组、CHD组TT基因型分别为130(76.0%)、75(74.3%)、103(70.1%),CT基因型分别为36(21.1%)、23(22.8%)、40(27.2%),CC基因型分别为5(2.9%)、3(2.9%)、4(2.7%),三组间比较差异无统计学意义(F=1.718,P＞0.05);Lp(a)基因rs6415084位点对照组、CAVD组、CHD组TT基因型分别为5(2.9%)、2(2.0%)、4(2.7%),CT基因型分别为33(19.3%)、20(19.8%)、32(21.8%),CC基因型分别为133(77.8%)、79(78.2%)、111(75.5%),三组间比较差异无统计学意义(F=0.551,P＞0.05);Lp(a)基因rs10455872位点对照组、CAVD组、CHD组AA基因型分别为171(100%)、99(98.0%)、147(100%),AG基因型分别为0(0.0%)、2(2.0%)、0(0.0%),三组间比较差异无统计学意义(P=0.058)。经logistic回归分析,与对照组相比, CAVD组及CHD组的Lp(a)水平更高,其差异有统计学意义,但未发现Lp(a)基因rs7770628及rs6415084两个位点的基因分布频率的差异有统计学意义(P>0.05)。线性回归结果表明,rs7770628以及rs6415084两个基因位点的基因分布均与Lp(a)水平升高有关。rs10455872位点只有2例SNP基因型为AG,且皆出现于CAVD组。结论 Lp(a)基因rs7770628、rs6415084位点的基因分布均与Lp(a)的升高有关,Lp(a)高表达与CAVD以及CHD患病具有相关性。     

Secondary sulphonylurea failure: what pathogenesis is responsible?

Sulphonylurea (SU) stimulates insulin secretion by pancreatic beta-cells and is generally used as a first-line treatment for type 2 diabetes. However, after long-term SU treatment (six months or over), some patients begin to show an increase in blood glucose once again (secondary SU failure). Two theories have been put forward to explain this failure--dysfunction of the proinsulin conversion machinery or insulin resistance. However, the primary pathogenesis behind secondary SU failure still needs to be investigated. Using a reliable technique that specifically identifies intact proinsulin (IPI), total proinsulin (TPI) and specific insulin (SI), this study aims to discover if a defect in the proinsulin converting mechanism plays a role in SU failure. Three groups were recruited for this study: healthy controls (n=8), SU responders (n=38) and secondary SU failures (n= 46). Serum concentrations of insulin-related molecules released in response to a standard glucose challenge test were compared between the groups. It was found that total SI was lower in the patient groups (P<0.05 compared to the control group), while TPI and IPI showed no distinct difference between the three groups (P>0.05). TPI:SI ratio and IPI:SI ratio showed marked increases in the patient groups (P<0.05 compared to control group), with no obvious quantitative difference between SU responders and secondary SU failures (P>0.05). Similar results for the Homa Insulin Resistant Index were found between the two patient groups. Interestingly, blood glucose at 180 mins after glucose challenge was significantly higher in the secondary SU failure group (P<0.05), with no correlation to SI, while the SU responder group showed good correlation between the parameters (P<0.05). We conclude that type 2 diabetes is associated with obvious dysfunction in the proinsulin-converting process and shows severe SI deficiency in responding to glucose challenge. Dysfunction of the proinsulin conversion mechanism was not an extra cause responsible for SU failure.     

Intracellular pH, intrauterine growth and the insulin resistance syndrome.

Defects of both sodium-hydrogen exchange (NHE) and sodium-lithium countertransport (SLC) have been described in subjects at increased risk of coronary heart disease (CHD). Sodium transport is linked to the regulation of cell volume, intracellular pH and cell growth, which may explain aspects of this association. However, impaired growth in early life is also linked to adult CHD, and 'programmed' alterations of cell behaviour are postulated to be responsible for this. In this study, therefore, we examined whether NHE or SLC in adults are predicted by anthropometric measures at birth, as well as being associated with insulin resistance syndrome (IRS) variables in adulthood. Red cell SLC was measured in 26 adults, and NHE in dermal fibroblasts from another 15 subjects characterized anthropometrically at birth. SLC activity correlated with LDL cholesterol, triglycerides and urate (r=0.42 - 0.49; 0.05 > P>0.01), but not birth anthropometry. NHE V(max) correlated with plasma insulin (r=0.80; P<0.001), but birth weight was unrelated to V(max), K(m) or Hill coefficient for H(i)(+). However, pH(i) correlated with birth weight (r=0.74; P=0.002), insulin sensitivity (r=0.52; P<0.05), fasting glucose (r=-0.52; P<0.05) 2 h insulin (r=0.51; P<0.05) 2 h glucose (r=-0.54; P<0.05). In conclusion, red cell SLC is related to IRS variables, but not with birth weight measures. In contrast, low intracellular pH(i) is related to both low birth weight and adult insulin resistance, suggesting it might be a 'programmed' cell phenotype, although this is not apparently explained by altered NHE kinetics.     

Association between homocysteinemia and renal function in patients with type 2 diabetes mellitus

Homocysteinemia is an independent risk factor for cardiovascular disease, but information on its association with type 2 diabetes and mild renal dysfunction is limited. Plasma total homocysteine (tHcy) concentration is partly determined by renal plasma clearance. Serum cystatin C (Cys C) concentration has been introduced as a marker of renal function, specifically as an indicator of glomerular filtration rate (GFR). The aim of this study was to explore the relationships among tHcy, creatinine clearance (Ccr), serum Cys C, and microalbuminuria in a population with type 2 diabetes. Fasting plasma tHcy, serum homocysteine-related vitamins (folate and vitamin B12), serum Cys C, serum creatinine, urine microalbumin, and creatinine clearance were determined in 75 type 2 diabetic patients and 40 healthy control subjects. The patients were assigned to two groups based on urinary albumin excretion (UAE): normoalbuminuric (NAU, UAE < 30 mg/24 hr, n = 35) and microalbuminuric (MAU, UAE 30-300 mg/24 hr, n = 40). Ccr was calculated using the Cockroft-Gault formula. Plasma Hcy levels were determined by HPLC with fluorescence detection and serum Cys C by automated particle enhanced immunoturbidimetry. Plasma tHcy levels were significantly higher in normoalbuminuric and microalbuminuric patients than in controls (10.64 +/- 0.53, 13.29 +/- 0.78, 6.91 +/- 0.37 mmol/L, respectively). Serum Cys C levels in microalbuminuric diabetics were higher than in normoalbuminurics and controls (1.36 +/- 0.06, 1.12 +/- 0.04, 1.10 +/- 0.06 mg/ L, respectively). Positive correlations were noted between tHcy and Cys C levels in normoalbuminuric and microalbuminuric diabetics (r = 0.72, r = 0.64, respectively). Homocysteine and creatinine concentrations were correlated in both diabetic groups (r = 0.89, r = 0.93, NAU and MAU, respectively). Elevated plasma total homocysteine concentrations in type 2 diabetics suggest an association between homocysteinemia and deterioration of renal function, evidenced by increased serum creatinine and Cys C, Ccr, and microalbuminuria. These findings implicate homocysteinemia in the relationship between diabetic nephropathy and cardiovascular complications of diabetes.     

血清C肽浓度测定的临床意义探讨

目的： 研究血清C肽浓度及胰岛素与C肽比值的临床意义。方法：用放射免疫分析测定2型糖尿病和肾功能不全患者血清C肽、胰岛素浓度,并计算胰岛素与C肽比值。结果：肾功能不全组病人血清C肽、胰岛素水平显著高于糖尿病各组,且胰岛素与C肽比值显著低于糖尿病各组（P〈0．01）;在糖尿病各年龄组中,胰岛素水平无明显变化（P〉0．05）;但血清C肽水平随年龄增大而升高,而胰岛素与C肽比值则显著下降（P〈0．01）。结论：测定血清C肽水平及胰岛素与C肽比值有助于了解糖尿病患者的肾功能状况,值得进一步深入探讨。     

谷氨酰胺对高脂饮食诱导C57BL/6J小鼠肥胖和胰岛素抵抗的影响

目的:探讨谷氨酰胺(L-glutamine,Gln)对高脂饮食(high-fat diet,HFD)诱导小鼠肥胖和胰岛素抵抗的影响。方法:60只雄性C57BL/6J小鼠随机分为正常对照(normal control,NC)组、HFD组、HFD+丙氨酸(Lalanine,Ala)组和HFD+Gln组,每组15只。每周记录小鼠体重,给药16周后禁食不禁水12 h测定空腹血糖(fasting blood glucose,FBG),处死后剖腹取附睾脂肪垫并称重。采用酶联免疫法检测小鼠胰岛素(insulin,INS)、瘦素(leptin,LEP)、脂联素(adiponectin,APN)和胰高血糖素样肽1(glucagon-like peptide-1,GLP-1)的水平,并计算胰岛素抵抗指数(insulin resistance index,IRI)和胰岛素敏感指数(insulin sensitivity index,ISI)。结果:与NC组比较,HFD组小鼠体重和附睾脂肪垫重量明显升高,FBG、INS、IRI和LEP水平均明显升高,ISI和APN水平明显降低(P0.05);与HFD组比较,HFD+Gln组小鼠体重明显下降,FBG和LEP水平明显降低,IRI明显减小(P0.05)。4组小鼠血清的GLP-1水平差异无统计学显著性。结论:谷氨酰胺减轻高脂饮食诱导的肥胖小鼠体重和胰岛素抵抗。     

Homocysteine and nitric oxide in patients undergoing diagnostic coronary angiography

We evaluated the plasma homocysteine (tHcy) and nitric oxide metabolites (nitrite plus nitrate; NOx) data of consecutive patients undergoing diagnostic coronary angiography (n=79) with respect to the presence and severity of coronary artery disease (CAD), the presence of acute coronary syndromes (ACS), and the risk status of patients. Hyperhomocysteinemia (>15 micromol/L) was detected in 11% of the controls (n=19) and 37% of CAD patients (n=60) (p=0.03). Plasma tHcy in CAD patients was not significantly different from controls, but those with 3-vessel disease had a significantly higher tHcy concentrations than did controls (p=0.049). The patients with 3-vessel disease and ACS had the highest concentrations of tHcy (16.9 +- 4.4 micromol/L), and the difference from the ACS patients with 1- and 2-vessel involvement was significant (p=0.03). In patients with 1-vessel involvement, tHcy was correlated with NOx (r=0.62, p=0.005); in patients with 2- and 3-vessel disease this correlation could not be observed. The high-risk patients (n=51) had a higher mean number of vessel involvement and tHcy (p<0.001, p<0.05, respectively) but lower NOx (p<0.05) when compared to the low-risk patients (n=28). It appears that in the early stages of atherosclerosis hyperhomocysteinemia causes an increase in NOx production, but with progression of the disease this compensatory increase disappears.     

胰岛素抵抗对糖尿病患者心功能的影响

目的:探究分析胰岛素抵抗对糖尿病患者心功能的影响.方法:选择2015年1月至2018年3月在我院内分泌科就诊的156例2型糖尿病患者进行回顾性分析,根据患者胰岛素抵抗指数将所有患者分为胰岛素抵抗组(胰岛素抵抗指数≥2.69,n=82),非胰岛素抵抗组(胰岛素抵抗指数<2.69,n=74),并选取同时期在我院体检的和78...