p66shc基因表达与老年糖尿病患者早期肾损伤的相关性

目的研究p66shc基因在老年糖尿病患者外周血单核细胞中的表达及其与早期肾损伤指标的关系。方法采用实时PCR技术检测74例老年糖尿病患者和48例健康老年人(对照组)外周血单核细胞中p66shc基因表达水平,结合临床资料分析p66shc与早期肾损伤指标尿微量白蛋白(m Alb)、转铁蛋白(TRF)、免疫球蛋白(Ig G)、α1-微球蛋白(α1-MG)和N-乙酰-β-D-氨基葡萄糖苷酶(NAG)之间的相关性。结果 p66shc基因在老年糖尿病患者中的表达水平显著高于对照组(P<0.05);与对照组相比,老年糖尿病患者m Alb、TRF、Ig G、α1-MG、NAG均显著升高(均P<0.01),并均与p66shc基因的表达水平呈正相关。结论 p66shc与老年糖尿病患者早期肾损伤密切相关,可为老年糖尿病患者肾损伤的早期诊断提供新的依据。     

白塞病外周血白细胞差异表达基因谱的发现和验证

目的 建立白塞病(BD)外周血白细胞差异表达基因谱,探讨BD致病基因.方法 应用Affymetrix寡核苷酸基因芯片研究3对未经治BD和健康人外周血白细胞,建立差异表达基因谱;从中选取B细胞淋巴瘤6(BCL6)、白细胞来源的精氨酸氨基肽酶(LRAP)、可诱导的T细胞共刺激分子配体(ICOSLG)和膜表面金属蛋白内切酶(MME)4个基因,设立BD组、健康组、系统性红斑狼疮(SLE)组和类风湿关节炎(RA)组,采用实时定量一聚合酶链反应验证其表达水平.结果 ①在国际上首次建立了BD外周血白细胞差异表达基因谱,包含差异表达基因146个,其中上调基因89个,下调基因57个.②上述4个基因表达水平在BD活动期均显著高于健康对照组,在缓解期下降;其中BCL6、MME表达水平也显著高于SLE组和RA组.结论 ①本研究为在基因水平上进一步揭示BD的发病机制提供了线索;②首次证实了上述4个基因的表达水平与BD的活动性有关;分析表明肿瘤坏死因子(TNF)-α和干扰素(IFN)-γ调控BCL6、ICOSLG和LRAP表达水平,可能是一个新发现的致病环节;MME基因可能成为利于BD诊断的检测标记.     

脑源性神经营养因子、TNF-α及巨噬细胞迁移抑制因子在抑郁症食蟹猴中枢边缘系统奖赏环路中的作用

目的探讨脑源性神经营养因子(BDNF)、肿瘤坏死因子(TNF)-α及巨噬细胞迁移抑制因子(MIF)在抑郁症食蟹猴中脑边缘奖赏环路中的作用。方法选取成年雌性食蟹猴12只,按照随机数字表法分为对照组(n=6)和实验组(n=6)。实验组食蟹猴于vertical-chamber拘禁笼中拘禁60 d,对照组食蟹猴仍群居于大笼中。定时观察两组动物行为时间,重点包括社会交流、进食、休息、焦虑、情感依附等时间,并注意有无外伤、疾病发生。分别在拘禁前、拘禁期间第10、30、60天、拘禁后10 d采集静脉血,检测两组各时间点BDNF、TNF-α及MIF含量。结果与对照组相比,实验组食蟹猴运动、探索和进食行为时间显著减少,抑郁行为持续时间较长(P<0.05)。与对照组相比,实验组食蟹猴BDNF含量降低,MIF及TNF-α含量增高(P<0.05);且实验组食蟹猴随着拘禁时间延长,BDNF含量逐渐降低,MIF及TNF-α含量逐渐升高(P<0.05)。结论增加BDNF含量、降低TNF-α及MIF含量,可能是中枢边缘系统奖赏环路减缓抑郁症的机制之一。     

PTE患者整合素相关mRNA差异性表达的意义

目的 检测肺血栓栓塞症(PTE)患者整合素相关mRNA表达水平,分析其差异表达的意义.方法 随机取选20例PTE患者为PTE组;另选20例年龄、性别与之匹配的非PTE患者为对照组.提取外周血单个核细胞总RNA,应用人类全基因组表达谱芯片比较两组整合素相关mRNA表达的差异,并进行FQ-PCR验证芯片的可靠性.差异基因筛选标准为P<0.05.结果 检测出白细胞相关整合素基因mRNA14条,PTE组mRNA表达部分高于对照组,主要为β1及β2组,差异具有统计学显著意义(P<0.05);血小板相关整合素基因mRNA11条,PTE组表达上调的整合素占分布于血小板的所有整合素的60%,主要为β1及β3组,有统计学显著意义(P<0.05);其他整合素相关基因mRNA11条中,亦有部分表达显著上调或下调(P<0.05),它们的主要配体均为纤维连接蛋白.结论 PTE中分布于白细胞以及血小板的大部分整合素表达异常上调,纤维连接蛋白相关整合素表达亦有显著改变,PTE可能与两者介导的炎症反应、血小板聚集相关.     

食蟹猴自发性膝骨关节炎模型的中药干预实验

目的分析独活寄生汤干预对食蟹猴自发性膝骨关节炎(KOA)模型炎症调节的作用,为进一步药物治疗的疗效检验及安全性评估提供可靠保证。方法选取清洁级青年型和老年型食蟹猴各6只,对食蟹猴自发性KOA模型进行评价;将老年型食蟹猴随机分为干预组和空白对照组,采用独活寄生汤进行干预,对比两组全血白细胞、C反应蛋白、红细胞沉降率及关节液性状和肿瘤坏死因子(TNF)-α含量的表达变化。结果老年型食蟹猴自发性KOA模型会出现典型与人类相似的骨关节炎相关指标改变。独活寄生汤干预可下调TNF-α表达,降低全血白细胞、C反应蛋白水平,干预前后差异有统计学意义(P0. 05)。结论老年型食蟹猴自发性KOA模型能有效模拟人类自发性KOA发生发展;独活寄生汤干预可能通过抑制TNF-α的表达,降低关节软骨的炎症因子水平,从而缓解KOA病程,产生治疗作用;全血白细胞、C反应蛋白可作为疗效判断的重要参考指标。     

基因芯片联合荧光定量PCR筛查主动脉夹层肺损伤标志物

目的:使用人表达谱基因芯片筛查主动脉夹层外周血白细胞差异基因表达,用荧光定量PCR进行验证主动脉夹层肺损伤标志基因。方法:分别抽取主动脉夹层患者和主动脉瘤患者外周血白细胞RNA,用基因芯片筛查差异表达基因,选取与肺损伤相关的基因。抽取主动脉夹层肺损伤和非肺损伤患者外周血白细胞RNA,用荧光定量PCR进行验证。结果:差异表达基因134个,其中78个为上调基因,56个为下调基因,差异基因主要涉及炎症反应、免疫反应、宿主防御、胶原蛋白调节、应激反应以及造血和细胞凋亡等多个生物学过程,用荧光定量PCR验证肺损伤相关基因,发现基质金属蛋白酶(MMP)-9在主动脉夹层肺损伤组明显升高(P<0.05)。结论:基因表达谱cDNA芯片是筛查主动脉夹层肺损伤差异基因的有效方法,差异基因可以进一步在荧光定量PCR中验证,MMP-9可用于主动脉夹层肺损伤的诊断和治疗。     

应用基因芯片检测系统性红斑狼疮患者外周血B淋巴细胞

目的 应用寡聚核苷酸基因表达芯片研究系统性红斑狼疮(SLE)患者与健康志愿者外周血B淋巴细胞基因表达谱的变化.方法 应用包含21522条70 mer长度Oligo DNA的寡聚核苷酸芯片(22K Human Genome Array)分别检测6例SLE患者和6名健康志愿者外周血B淋巴细胞基因表达谱,应用聚类分析法分析差异表达的基因.结果 SLE患者外周血B淋巴细胞和健康志愿者B淋巴细胞之间基因表达谱有显著差异,芯片中聚类表达显著上调的基因15个,主要包括Ⅰ型干扰素(IFN)通路中的相关分子;聚类表达显著下调的基因22个,主要包括神经内分泌相关的精氨酸甲基化转移酶家族等与雌激素代谢相关的基因.进一步对这些差异表达基因进行了初步的功能分类分析,分析结果表明这些基因主要与B淋巴细胞的JAK-STAT信号通路和激素代谢相关.结论 SLE患者外周血B淋巴细胞基因表达谱存在显著差异,芯片显示氨基酸代谢、激素代谢、细胞增殖和凋亡、炎症反应等相关生物学功能的改变可能参与SLE的发病.     

G6PC基因在糖尿病患者中的表达及其与糖尿病肾病发生的相关性

目的探讨糖尿病(DM)患者外周血白细胞中葡萄糖-6-磷酸脱氢酶(G6PC)基因的表达变化及其与糖尿病肾病(DN)发生的相关性。方法选取30例DM患者作为实验组(其中10例DN患者),20例健康体检者为对照组,采用RT-PCR法检测DM患者外周血白细胞G6PC mRNA表达水平(以β-actin为内参),同时比较DN患者与肾功能正常DM患者之间G6PC mRNA表达差异。结果与对照组比较,DM组患者G6PC的mRNA表达明显降低(0.65±0.19 vs 1.54±0.32,P<0.05)。DN组G6PC mRNA表达量显著低于肾功能正常DM组患者(P<0.05)。结论 DM患者外周血白细胞G6PC基因表达下降,其可能在DN发生及进展中具有重要作用。     

普罗布考对2型糖尿病合并冠心病患者外周血单核细胞Toll样受体4/核转录因子κB信号通路的影响

目的 研究普罗布考对2型糖尿病患者外周血单核细胞Toll样受体4/核因子kB信号转导通路的影响,以进一步探讨普罗布考抗动脉粥样硬化机制.方法 选择85例2型糖尿病合并冠心病患者,随机分为对照组和治疗组:对照组按常规治疗,治疗组在常规治疗基础上加用普罗布考0.375 g,每天2次,口服,总疗程为24周.运用Real-time PCR、Western blotting方法分别测定治疗前后外周血单核细胞Toll样受体4、核因子kB mRNA和蛋白表达水平;ELISA检测外周血血清中白细胞介素1β的表达水平.结果 普罗布考显著降低2型糖尿病合并冠心痛患者总胆固醇、甘油三酯、低密度脂蛋白胆固醇和氧化型低密度脂蛋白水平,显著下调外周血单核细胞Toll样受体4 mRNA和蛋白的表达(P<0.05),明显减少核因子kB蛋白的表达,且显著抑制白细胞介素1β的生成(P<0.05).结论 普罗布考抗动脉粥样硬化除了降脂作用外,抑制外周血单核细胞Toll样受体4/核因子kB信号转导通路的激活,也可能是其抗炎、抗动脉粥样硬化的重要机制之一,提示普罗布考对防治2型糖尿病并发动脉粥样硬化这类患者有一定的作用.     

下肢动脉粥样硬化斑块内miRNA-199a-3p对外周血单核细胞的影响

目的探讨下肢动脉粥样硬化斑块内miRNA-199a-3p对外周血单核细胞的影响。方法选取37例下肢动脉粥样硬化闭塞症(AS)患者外周血为AS组。另外选取同期37名健康体检者外周血为对照组。新鲜血管组织取自1例下肢AS患者截肢远端血管为实验组,以其截肢近端血管为对照。实时荧光定量PCR检测新鲜血管组织,分离得到的外周血中单核细胞和微泡中miRNA-199a-3p表达水平。以人单核细胞TTHP-1为载体,miRNA-199a-3p mimics组和miRNA-199a-3p inhibitor组分别转染miRNA-199a-3p mimics和miRNA-199a-3p inhibitor,同时设置空白对照组。实时荧光定量PCR检测各组miRNA-199a-3p、趋化因子单核细胞趋化蛋白(MCP)-1、调解活化正常T细胞表达和分泌的趋化因子(RANTES)和Fractalkine表达水平。结果下肢动脉粥样硬化斑块内miRNA-199a-3p表达水平显著高于正常组织(P<0.05)。AS组外周血单核细胞和微泡中miRNA-199a-3p表达水平均显著高于对照组(P<0.05)。与空白对照组相比,miRNA-199a-3p mimics组miRNA-199a-3p表达水平显著上升(P<0.05),miRNA-199a-3p inhibitor组miRNA-199a-3p表达水平显著下降(P<0.05)。与空白对照组相比,miRNA-199a-3p mimics组MCP-1、RANTES和Fractalkine的mRNA表达水平显著降低(P<0.05),miRNA-199a-3p inhibitor组MCP-1、RANTES和Fractalkine的mRNA表达水平显著上升(P<0.05)。结论动脉粥样硬化斑块内巨噬细胞高表达miRNA-199a-3p,并以微泡形式分泌到外周血中,抑制单核细胞中MCP-1、RANTES和Fractalkine等趋化因子的表达,是一种动脉粥样硬化保护因素。     

Metabolism of apolipoprotein B in members of a family with accelerated atherosclerosis: influence of apolipoprotein E-3/E-2 pattern.

Familial combined hyperlipidemia (FCHL) appears to be the most common, simply inherited hyperlipidemia strongly associated with coronary heart disease. In the family examined in this study, two of the siblings who met diagnostic criteria for FCHL had extensive clinical atherosclerosis before age 30, unusually premature for this form of hyperlipidemia. Lipoproteins and low-density lipoprotein (LDL) apolipoprotein (apo) B metabolism were characterized in these siblings in an attempt to gain insight into the cause of the rapid atherosclerosis in the two siblings so affected. LDL apo B production rates were very high in all three siblings (25 to 30 mg/kg/d), consistent with FCHL. beta-Very-low-density lipoprotein-beta (beta-VLDL) was present in the plasma of both siblings with accelerated atherosclerosis. The isoapolipoprotein E pattern in both of these siblings was E-3/E-2. In the third sibling, who was free of premature clinical atherosclerosis and lacked plasma beta-VLDL, the pattern was E-3/E-3. Thus, the heterozygote apo E-3/E-2 pattern may be related to the accumulation of beta-VLDL in persons with a very high apo B production rate. The abnormal accumulation of beta-VLDL may be one of the possible explanations for the rapid, premature atherosclerosis in the two siblings with FCHL in this kindred. Both male members in this kindred also had low levels of high-density lipoproteins, and thus may have had an additional risk of developing atherosclerosis due to this lipoprotein abnormality as well.     

Plasma vascular endothelial growth factor and its receptor Flt-1 in patients with hyperlipidemia and atherosclerosis and the effects of fluvastatin or fenofibrate

Increased vascular endothelial cell growth factor (VEGF) may be important in cardiovascular pathophysiology (perhaps relating to angiogenesis and collateral vessel development) and binds target endothelium via receptors such as Flt-1. We hypothesized that there would be increased levels of plasma VEGF and Flt-1 in patients with atherosclerosis and others with hyperlipidemia compared with controls, and a reduction in these factors with 3 months of lipid-lowering therapy. Twenty patients with uncomplicated hyperlipidemia but no atherosclerosis, 20 patients with hyperlipidemia plus clear atherosclerosis, and 40 matched controls were studied. Plasma VEGF was higher in patient groups than in healthy controls (p <0.01), but Flt-1 was not significantly altered. After lipid-lowering therapy, patients with uncomplicated hyperlipidemia had significantly reduced total cholesterol and VEGF (all p <0.05) but no significant change in Flt-1. Lack of a significant correlation between the von Willebrand factor and VEGF suggests the latter is unrelated to endothelial damage. Plasma VEGF that increases in patients with uncomplicated hyperlipidemia free of major underlying atherosclerosis and in patients with hyperlipidemia plus established atherosclerosis is reduced by successful lipid-lowering treatment. These findings may have implications for the pathophysiology and treatment of hyperlipidemia and atherosclerosis, and suggest an alternative mechanism (i.e., modulation of angiogenesis) by which lipid-lowering therapy may reduce cardiovascular events beyond lipid reduction alone.     

Correlation of atherosclerosis between different topographic sites is highly dependent on the type of hyperlipidemia

There is a surprising paucity of studies that provide quantitative correlative data on the extent of atherosclerosis between different topographic sites. The impact of cardiovascular risk factors is dependent on the vascular bed, which underlies site-selective effects on progression of atherosclerosis. Therefore, the intraindividual correlation of atherosclerosis between different topographic sites may be dependent on the specific cardiovascular risk profile. The focused objective of the current study is to evaluate whether the correlation of the extent of atherosclerosis between different topographic sites is dependent on the type of hyperlipidemia. Atherosclerosis was quantified at four different topographic locations in the aorta of rabbits with type II or type III hyperlipidemia. Correlation coefficients and semi-partial correlation coefficients adjusted for plasma lipoproteins and sex were determined to compare the degree of atherosclerosis at different topographic sites. Semi-partial correlations adjusted for total plasma cholesterol, plasma triglycerides, and sex of the intima/media ratio between different topographic sites were highly dependent on the type of hyperlipidemia. E.g., the semi-partial correlation coefficient between the intima/media ratio at the level of the ascending aorta and at the level of the descending thoracic aorta was 0.87 (p < 0.0001) in the model of type II hyperlipidemia and was only 0.10 (p = NS) in the model of type III hyperlipidemia. This divergent pattern was also observed for other intersite correlations. Semi-partial Pearson correlation coefficients were very similar to unadjusted Pearson correlation coefficients. Correlation of atherosclerosis between different topographic sites may vary importantly in relation to the type of hyperlipidemia.     

硝苯吡啶对高脂血症家兔和患者脂质代谢的影响

本文观察了硝苯吡啶(Nif)对实验性高脂血症、动脉粥样硬化家兔脂质代谢的影响。结果表明,Nif对喂饲胆固醇(Ch)家兔有显著降低血浆总胆固醇、甘油三酯、低密度脂蛋白Ch、载脂蛋白B,升高血浆高密度脂蛋白Ch(HDL-Ch)及其亚类HDL_2-Ch,减少主动脉组织Ch、epoB沉积和粥样病变面积的作用。并观察了37例高血压病伴高脂血症患者,其口服Nif治疗后其血脂变化与动物实验结果一致。Nif影响脂质代谢的机制可能与Nif能加强低密度脂蛋白(LDL)受体途径处理LDL有关。     

Mutations in Japanese subjects with primary hyperlipidemia--results from the Research Committee of the Ministry of Health and Welfare of Japan since 1996--

Primary hyperlipidemia is caused by various molecular defects in lipid metabolism. The Research Committee on Primary Hyperlipidemia organized by the Ministry of Health and Welfare of Japan (present: the Ministry of Health, Labour and Welfare) has investigated reported mutations in Japanese patients with primary hyperlipidemia and related disorders (including hypolipidemia), and has created a database based on the questionnaire sent to the members of council board of the Japan Atherosclerosis Society. Mutations in the following genes were investigated: low density lipoprotein receptor, lecithin: cholesteryl acyltransferase, lipoprotein lipase (LPL), hepatic lipase, apolipoproteins A-I, A-II, A-IV, B, C-II, C-III and E, microsomal triglyceride transfer protein, and cholesterol ester transfer protein (CETP). Until 1998, 922 patients with primary hyperlipidemia and related disorders has been registered with the Research Committee, and 190 mutations in 15 genes had been reported, showing a marked variation in Japanese patients with primary hyperlipidemia and related disorders. So-called "common mutations" have been described in Japanese patients with familial hypercholesterolemia, LPL deficiency and CETP deficiency. The genetic defect of familial combined hyperlipidemia (FCHL) is still unknown although FCHL is speculated to be the most prevalent genetic hyperlipidemia, and further investigations should be performed to elucidate the molecular mechanisms of FCHL     

Enhanced in vivo platelet release reaction and malondialdehyde formation in patients with hyperlipidemia

Plasma level of beta-thromboglobulin (beta TG), a useful marker of in vivo platelet "release reaction,"was determined by radioimmunoassay in 69 patients, with three types of primary hyperlipidemia (IIa, IIb, IV) and compared with the findings in age- and sex-matched healthy controls and 57 patients with established atherosclerosis and peripheral vascular disease. Malondialdehyde (MDA) formation, used for assessment of prostaglandin synthesis, was determined in 51 and plasma platelet factor 4 (PF4), measured by radioimmunoassay, in 48 of the patients with hyperlipidemia. Results were correlated to five serum lipids and lipoprotein levels in the patients with hyperlipidemia. beta TG was significantly increased in the patients with hyperlipidemia and peripheral vascular disease, compared to those in the controls (p < 0.001); it was significantly higher in the patients with hyperlipidemia than in those with peripheral vascular disease. PF4 and MDA formation were also increased in the patients with hyperlipidemia, and significantly higher levels of MDA were obtained in patients with type IIb and type IV hyperlipidemia than in those with type IIa hyperlipidemia (p < 0.02). beta TG and MDA correlated weakly with total serum cholesterol triglycerides and very low density lipoprotein-triglyceride. There was also a significant correlation between beta TG and PF4, and MDA production. These results indicate that in vivo platelet "release reaction" and MDA formation are increased in hyperlipidemic patients. The release reaction is more enhanced in those with hyperlipidemia than in the patients with peripheral vascular disease. They suggest that the abnormal platelet function is related to the elevated levels of serum lipids and lipoproteins in the hyperlipidemic patients and not only to the atherosclerotic changes associated with hyperlipidemia.     

Genomic analysis of the response of mouse models to high-fat feeding shows a major role of nuclear receptors in the simultaneous regulation of lipid and inflammatory genes

The mechanisms of diet induced hyperlipidemia and atherosclerosis have been widely studied by delineating the role of candidate genes in transgenic and gene targeted mouse models. However, diet induced hyperlipidemia represents a complex process determined by many lipid genes that is only partly understood. This study is aimed at delineating the events induced by dietary intervention in different mouse models at the level of gene expression using microarray analysis. The focus is on the liver as the organ primarily responding to diet, and crucial in determining plasma lipid levels. Firstly, the effect of the genotype was studied. Expression profiles of liver genes were compared between APOE3Leiden (E3L), APOE knockout (E-/-) and C57BL/6JIco (B6) mice using the Incyte GEM 2.03 array carrying 9552 genes. Several hundred differentially expressed genes were identified indicating that the genotype alone effects gene expression. Secondly, the response of E3L mice to high-fat feeding was investigated using a mild and severe high-fat diet (diet W and N, respectively). Diet W caused differential regulation of 200 genes, while diet N affected the expression of 788 genes in B6 and 1010 genes in E3L mice. Annotation of these genes using the Gene Ontology (GO) database showed that two major processes were strongly affected by genotype and diet, namely lipid metabolism and inflammation, the latter as determined by "immune/defense response and detoxification" processes. Many nuclear receptor target genes were differentially regulated, with the largest effects modulated by the severe high-fat diet N, leading to the suppression of genes involved in bile acid, sterol, steroid, fatty acid, and detoxification metabolism. Strikingly, a substantial part of these nuclear receptor target genes were commonly regulated during the different experimental conditions. The common regulation of many nuclear receptor target genes underlying lipid and detoxification processes as found in this study, suggest a defense mechanism involving many nuclear receptors to protect against the accumulation of toxic endogenous lipids and bile acids. These results further strengthen the close link between hyperlipidemia and inflammatory processes.     

益气活血剂对兔胸主动脉粥样硬化形成的作用

目的探讨中药益气活血剂对高脂饮食兔动脉粥样硬化的预防及其作用机制。方法取纯种新西兰大白兔50只,随机分为4组:正常对照组、高脂模型组、益气活血预防组及益气活血治疗组,观察时间为2月。治疗前后检测血脂,治疗结束后分别取主动脉组织作脂质定量,测胸主动脉粥样硬化斑块面积和内膜、血管壁厚度等。结果①益气活血剂治疗可以降低高脂模型组血胆固醇、甘油三酯、低密度脂蛋白胆固醇,其中甘油三酯水平显著降低(P<0.01)。②益气活血剂治疗可减少高脂模型组动脉粥样硬化的形成,使内膜面积、厚度减少(P<0.05),但对管腔面积无明显影响(P>0.05)。③镜下观察发现,高脂模型组主动脉弓内膜充满泡沫细胞,壁上可见明显的粥样斑块;益气活血治疗组动脉壁脂质沉积相对较轻。结论益气活血剂具有降低血脂和抑制动脉粥样硬化形成的作用。     

糖尿病结合高脂血症对颈部动脉粥样硬化影响的超声分析

目的探讨应用超声分析评价糖尿病结合高脂血症时对颈部动脉粥样硬化的影响。方法选择该院2018年6月—2020年5月期间收治的108例糖尿病结合高脂血症患者列为A组,以同期收治的105例单纯2型糖尿病患者以及100名体检健康者分别列为B组和C组,分别进行超声检查,观察各组生化指标差异,分别测量颈总动脉内-中膜厚度(IMT)、颈总动脉分叉内膜厚度(BIMT),计算斑块检出率。结果A、B组的TC、TG、LDL及HbA1c等生化指标显著高于C组,以A组最高;并且,A、B组的IMT、BIMT以及斑块检出率也均高于C组,并以A组最高,组间差异有统计学意义(P<0.05)。结论糖尿病可能是造成动脉粥样硬化的独立危险因素,合并高脂血症可以加重颈部动脉粥样硬化的程度,降低了血管弹性,提高了血管阻力。