海南部分地区与省外非转移性浸润性乳腺癌患者临床病理参数的对比分析

目的:分析海南部分地区(省内)与省外非转移性浸润性乳腺癌患者临床病理参数的异同。方法:收集我院自2012年6月-2017年6月经病理和影像学确诊的非转移性浸润性乳腺癌患者214例,筛选有效病例159例,将患者年龄、肿瘤位置、ScarffBloom and Richardson(SBR)分级、肿瘤标记物(CEA、CA125、CA153)、TNM分期、阳性/活检淋巴结数、lunimal分型、初潮年龄、绝经状态、生育子女数、体重指数、体表面积等数据按省内、省外进行统计分析。结果:①省内患者确诊年龄明显早于省外(47.48±10.05 vs 51.33±10.03,p=0.02);②省内患者具有生育子女数较多(1.93±0.97 vs 1.38±0.64,p=0.00)和活检淋巴结数较多(20.67±9.56 vs 18.00±6.74,p=0.04)的特征;③省内患者绝经后体重指数(22.66±3.24 vs 25.56±3.67,p=0.00)和体表面积(1.60±0.12 vs1.68±0.16,p=0.00)较绝经前明显上升,而省外患者此现象不明显。结论:海南部分地区非转移性浸润性乳腺癌患者具有发病年龄早等特点,绝经后体质改变可能为该地区乳腺癌的促发因素。     

脉搏波传导速度检测在评价高血压病患者大动脉弹性中的应用 与影响因素分析

目的:探讨脉搏波传导速度(PWV)检测在评估高血压病患者大动脉弹性中的应用价值与影响因素分析 方法:采用分层整体抽样法随机抽取高血压病患者2178例,同时抽取非高血压2182人作为对照组.应用Complior SP VP-1000动脉硬化检测仪测定颈一股动脉脉搏波传导速度(C-FPWV)评估大动脉弹性.采用多元逐步线性回归分析性别、年龄、体质指数(BMI)、收缩压(SBP)、舒张压(DBP)、总胆固醇(TC)、甘油三脂(TG)、空腹血糖(FPG)和尿酸(UA)等指标与高血压痛患者大动脉弹性下降的影响因素.结果:C-FPWV平均值高血压组(1594± 264cm/s)显著高于对照组(1216± 231cm/s),两组差异有显著性意义(X2=31.659,P=0.00).＞40岁各年龄段PWV值上升程度,高血压组明显高于对照组(X2＝ 18.954～36.924,P=0.00),两组PWV值上升程度与年龄呈正相关.多元逐步线性回归分析表明:BMI≥28kg/m2、SBP≥ 140mmHg、DBP≥90mmHg、TC＞5.28± 0.62 mmol/L、TG＞ 1.68± 0.64mmol/L等指标高血压组明显高于对照组(t=14.314～17.428,P＜0.05).在性别、UA和FPG等指标两组无明显差异(X2=6.368～13.618,P＞0.05).结论:高血压痛患者PWV值上升程度显著高于非高血压者,BMI、SBP、TG、TC是高血压病患者大动脉弹性下降的主要影响因素.PWV值可作为评价大动脉弹性的可靠指标.     

兰州地区健康体检者血脂水平分析

目的:通过检测兰州地区健康体检者空腹血脂水平了解本地区人群血脂水平现状及血脂异常情况,建立本地区血脂参考值。方法:采用全自动生化分析仪检测兰州市2328名健康体检者,血清胆固醇(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)。比较不同年龄、性别血脂水平差异。结果:本地区2328名被检者,女性TC平均(4.54±0.94)mmol/L,TG中位数1.24mmol/L、HDL-C平均(1.34±0.26)mmol/L、LDL-C平均(2.61±0.76)mmol/L;男性TC平均(4.52±0.84)mmol/L、TG中位数1.56mmol/L mmol/L、HDL-C平均(1.20±0.23)mmol/L LDL-C平均(2.76±0.72)mmol/L,血脂水平随年龄增加逐渐升高(P<0.05)。血脂参考范围为女性TC:2.70~6.38 mmol/L、TG:0.52~3.66 mmol/L、HDL-C:0.83~1.85 mmol/L、LDL-C:1.12~4.10 mmol/L男性:TG:2.87~6.17 mmol/L、0.65~4.00 mmol/L、0.75~1.65 mmol/L、1.35~4.17 mmol/L。男性高TC、高TG、低HDL-C和高LDL-C患病率为18.2%、42.8%、19.6%和28%,女性高TC、高TG、低HDL和高LDL的患病率分别为22.1%、25.5%、2.7%和23.5%。结论:兰州地区血脂水平随年龄、性别、地区不同存在较大差异,临床上不能采用统一标准衡量,而应根据本地区建立的参考值诊断高脂血症。积极控制血脂水平、降低高脂血症患病率预防心脑血管疾病发生。     

中国北方地区血清钙、维生素D水平与乳腺癌的相关性研究

目的:探讨中国北方地区血清钙、维生素D水平与乳腺癌及相关临床因素的关系.方法:选取2007年12月至2012年7月哈尔滨医科大学附属肿瘤医院794例女性乳腺癌患者及976例乳腺良性肿瘤患者,并以128例健康妇女为对照,取空腹血清采用原子吸收分光光度法检测三组血清钙含量,采用放免法检测三组中162例血清25(OH)D含量,结合相关临床资料进行分析.结果:乳腺癌组血清钙含量为2.26± 0.12 mmol/L,乳腺良性肿瘤组血清钙含量为2.26±0.09 mmol/L,正常对照组血清钙含量为2.25±0.24 mmol/L,经方差分析,三组总体均数差别无统计学意义(P＞0.05);乳腺癌患者的血清钙水平与年龄、TNM分期、BMI、绝经情况、乳腺癌家族遗传史无关(P＞0.05).乳腺癌组血清25(OH)D含量为41.91±7.55 ng/mL,乳腺良性肿瘤血清25(OH)D含量为54.62±7.48 ng/mL,正常对照组血清25(OH)D含量为56.15±8.87 ng/mL,经方差分析,乳腺癌患者血清25(OH)D含量低于乳腺良性肿瘤组,差别有统计学意义(P＜0.05),乳腺良性肿瘤组与正常对照组差别无统计学意义(P＞0.05);乳腺癌患者的维生素D水平与年龄、TNM分期、BMI、绝经情况有关(P＜0.05),而与乳腺癌家族遗传史无关(P＞0.05).结论:中国北方地区的乳腺癌患者血清钙水平与乳腺良性肿瘤患者无明显差异.乳腺癌患者的维生素D水平低于乳腺良性肿瘤患者,并且与年龄、TNM分期、BMI、绝经情况有关.维生素D水平降低可能与乳腺癌的发生有关,高水平的维生素D可能会降低女性患乳癌的风险.     

中老年男性患者血脂代谢特点及与年龄等因素的相关分析

目的:探讨中老年男性患者血脂代谢特点及与年龄等因素的相关性。方法:资料来自2006年6月于我院干部门诊进行健康查体的1603例中老年男性患者(排除正在服用降脂药物的患者),采用全自动生化分析仪对血清总胆固醇(TC)、血清甘油三酯(TG)、血清低密度脂蛋白胆固醇(LDL-c)、血清高密度脂蛋白胆固醇(HDL-c)、空腹血糖(FBG)、血肌酐(Cr)及血尿酸(UA)等指标进行测定,同时记录身高、体重及血压等基本资料。结果:入选患者血脂异常总检出率为56.27%,其中TC、TG、HDL-c及LDL-c异常检出率分别为36.74%、28.20%、10.79%及6.92%,以TC、TG异常为主。与50~59岁组相比,80岁以上高龄老年组TG异常及HDL-c异常检出率显著降低,TC及TG水平显著降低,HDL-c水平显著升高(P<0.05)。在校正BMI、SBP、DBP、UA、FBG及CCr等危险因素影响后的多元线性回归分析发现,年龄每升高10岁,TC、TG分别降低约0.097 mmol/L及0.087 mmol/L,HDL-c升高约0.113 mmol/L。结论:中老年男性患者血脂异常以高TC和高TG为主,TC、TG与年龄呈负相关,HDL-c与年龄呈正相关,需针对高龄老年患者血脂代谢特点进行合理调脂治疗。     

应用降糖通脉胶囊联合运动锻炼可改善老年肥指标和抑郁情绪

为了探讨降糖通脉胶囊联合运动锻炼对老年肥胖患者肥胖指标、抑郁情绪的影响,本研究选取了2015年1月至2016年10月我院120例老年肥胖患者,随机分为观察组和对照组,各60例,对照组在接受西医常规治疗基础上进行同步运动锻炼,观察组加用降糖通脉胶囊治疗,疗程均为14 d。观察2组临床疗效、肥胖指标、空腹血糖(FBG)、餐后2 h血糖(2hPG)及糖化血红蛋白(HbAlc),比较两组患者治疗前后生活质量、抑郁评分。研究发现,治疗组总有效率为96.7%(58/60),对照组为83.8%(50/60),两组比较差异有统计学意义(χ2=11.23, p0.01);观察组BMI、WHR、腹围及股围显著低于对照组,差异有统计学意义(p0.01);治疗后,观察组躯体功能((59.15±9.51)比(55.12±4.36), t=7.03)、心理功能((72.25±3.18)比(65.08±5.31),t=8.36)、社会功能((70.14±8.57)比(68.00±6.46), t=6.38)评分高于对照组(p 0.05);治疗后FBG ((6.5±1.4)mmol/L比(8.2±1.7) mmol/L, t=8.05)、2hPG ((8.6±2.1) mmol/L比(11.3±2.5) mmol/L, t=7.84)、HbAlc ((5.1±1.0)%比(6.4±1.5)%, t=6.38)水平低于对照组(p0.05);治疗后观察组HAMA ((9.35±2.21)比(11.43±2.08), t=7.31)、HAMD评分((9.09±2.38)比(11.53±3.31), t=8.35)低于对照组(p0.05)。研究表明,降糖通脉胶囊联合运动锻炼治疗老年肥胖患者效果显著,能有效降糖降脂,降低肥胖指标,改善生活质量及抑郁情绪,值得推广。     

青少年家族性高胆固醇血症患者血浆同型半胱氨酸和高敏C 反应蛋白水 平的临床价值及与血脂相关性研究

目的:探讨血浆同型半胱氨酸(Homocysteine,Hcy)、高敏C反应蛋白(Hypersensitive C-reactive protein,hs-CRP)在家族性高胆固醇血症(FH)的纯合子和杂合子患者中的水平及其与临床生化指标的相关性。方法:入选在2013.10~2015.7期间在动脉硬化门诊随访、确诊的家族性高胆固醇患者34人(纯合子14例,杂合子20例)。根据FH纯合子、杂合子、健康体检者分成三组,分别测定其总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、空腹血糖(Glu)、Hcy、hs-CRP水平,并比较FH患者血浆LDL-C、非高密度脂蛋白(non-HDL)水平Hcy、hs-CRP水平的相关性。结果:FH组的TC、LDL-C、non-HDL、Hcy水平显著高于正常对照组(P0.05)。FH根据基因型亚组分析中,青少年纯合子组HDL-C[(0.78±0.21)vs(1.25±0.40)mmol/L]小于杂合子组(P0.001),而TC[(16.11±2.66)vs(7.30±2.54)mmol/L]、LDL-C[(14.06±2.22)vs(5.25±2.16)mmol/L]、non-HDL[(15.33±2.60)vs(6.05±2.61)mmol/L]、Hcy[(19.3±11.58)vs(11.29±3.42)μmol/L]水平显著高于杂合子组(P0.05)。Pearson相关性分析显示,FH患者血浆LDL-C、non-HDL水平与Hcy水平呈正相关(P0.05),而与hs-CRP无相关性。结论:FH患者,特别是青少年的纯合子患者,与对照组相较,具有较高的TC、LDL-C和Hcy水平,并且与血浆LDL-C、non-HDL水平呈正相关。FH患者hs-CRP的水平高于健康人,但差异无统计学意义,与血浆LDL-C、non-HDL水平也无明显相关性。     

Nucleobindin-2 在乳腺癌中表达的临床病理意义

目的:探讨NUCB2在乳腺癌中的表达及临床病理意义。方法:收集乳腺癌病例及相应的临床资料包括随访资料应用免疫组织化学技术检测良性病变,有/无淋巴结转移的乳腺癌及配对淋巴结转移灶中NUCB2的表达,分析NUCB2表达与乳腺癌临床病理指标和生存状态间的关系。结果:免疫组化结果:显示NUCB2在BBD、MBC、NMBC、PMLN的阳性表达率分别为90.0%(45/50),82.1%(87/106)、48.2%(40/83)、47.2%(50/106)。其中,NUCB2在BBD的阳性表达率显著高于NMBC、PMLN,而与MBC无显著性差异;在MBC中的阳性表达率显著高于NMBC;在MBC中的阳性表达率显著高于PMLN。临床病理分析结果:显示乳腺癌原发灶中NUCB2表达与淋巴结转移(p=0.000)、临床分期(p=0.001)、雌激素阳性表达(p=0.020)具有显著性相关。而与年龄、肿块大小、组织学分级、组织学类型、孕激素受体、HER2表达、绝经情况无显著相关。Kaplan-Meier分析结果:显示NUCB2阳性表达病例的总生存率比阴性病例更短(P=0.004)。结论:NUCB2在乳腺癌中表达与淋巴结转移、临床分期、雌激素受体表达和生存状态相关,可能在乳腺癌恶性演进和预后中具有重要意义。     

Leptin、TNF-α、FFA在肥胖症患者血清中的表达及临床意义

目的:研究瘦素(Leptin)、肿瘤坏死因子α(TNF-α)和游离脂肪酸(FFA)在肥胖患者血清中的表达以及其临床意义。方法:选取2013年5月到2014年5月我院体检的肥胖症患者30例(研究组),另选取非肥胖症者30例(对照组),测量两组空腹血糖(FPG)、空腹胰岛素(FINS)、血脂和Leptin、TNF-α、FFA等指标,并比较两组之间的差异,观察Leptin、TNF-α、FFA和肥胖相关指标的相关关系。结果:研究组甘油三脂(TG)、极低密度脂蛋白-胆固醇(VLDL-C)、Leptin、FINS、FPG、TNF-α、FFA以及HOMA模型胰岛素抵抗指数(HOMA-IR)分别为(1.98±0.31)mmol/L、(0.76±0.02)mmol/L、(15.14±0.04)μg/L、(20.56±0.04)mmol/L、(5.93±0.04)mmol/L、(43.98±0.14)ng/L、(0.17±0.01)mmol/L和(5.37±0.25)均显著高于对照组,两组比较差异具有统计学意义(t=9.423,8.979,9.074,10.082,9.089,9.562,9.065,10.083,均P0.05);研究组胰岛素敏感指数(ISI)为(0.011±0.002)显著低于对照组(0.021±0.001),两组比较差异具有统计学意义(t=11.428,P=0.012);FFA与TG、HOMA-IR、FINS呈正相关关系(r=0.842,0.796,0.879,P=0.017.0.019,0.023),与ISI呈负相关关系(r=-0.958,P=0.021);Leptin与BMI、HOMA-IR、FINS呈正相关关系(r=0.793,0.869,0.837,P=0.018,0.022,0.017),与ISI呈负相关关系(r=-0.905,P=0.011);TNF-α与ISI呈负相关关系(r=-0.807,P=0.013)。结论:肥胖者血清中Leptin、TNF-α、FFA显著高于正常者,且和肥胖等项指标具有相关关系。     

鱼油对高脂喂养加小剂量STZ诱导的2型糖尿病大鼠血脂及肝脏的影响

目的:探讨鱼油对高脂喂养加小剂量STZ诱导的2型糖尿病大鼠脂代谢及肝脏组织的影响及其机制。方法:Sprague-Dawley大鼠随机分为对照组(Control)、高脂组(HF)、糖尿病组(DM)、高脂鱼油组(HF+FO)和糖尿病鱼油组(DM+FO),观察大鼠周体重变化,检测各组大鼠血糖、血脂、肝脏细胞形态学及过氧化损伤情况,探讨其可能的作用机制。结果:与对照组相比,高脂喂养大鼠体重明显增加(387.74±36.20 g vs 339.64±10.41 g,P0.05),血甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,TC)和低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)分别由1.96±0.06 mmol/L、1.91±0.09 mmol/L和0.72±0.07 mmol/L升高至2.29±0.16 mmol/L、2.08±0.06 mmol/L和1.22±0.09 mmol/L,高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)降低(0.92±0.15 mmol/L vs 1.80±0.07 mmol/L,P0.05),膳食添加鱼油后均有明显改善。糖尿病大鼠体重减轻(287.78±16.11 g vs 339.64±10.41 g,P0.05);但血清中LDL-C水平升高至1.08±0.08 mmol/L,HDL-C水平降低至1.09±0.07 mmol/L(P0.05),鱼油可显著提高HDL-C的水平(P0.05)。高脂组和糖尿病组均有明显的肝脏脂肪浸润和过氧化损伤,添加鱼油后明显减轻。结论:膳食添加鱼油对高脂膳食及2型糖尿病引起的血脂异常均有保护作用,可降低血中甘油三酯和低密度脂蛋白胆固醇水平;减轻大鼠肝脏脂肪浸润和过氧化损伤。     

Prevalence of coronary heart disease risk factors in a Cambridge, UK study

This paper examines the distribution and prevalence of risk factors for coronary heart disease in a sample of 165 men and 202 women over 40 years of age who had earlier participated in a coronary prevention trial from a general practice in Cambridge, UK. No significant differences were observed in total cholesterol levels between men and women, and a quarter of the sample had concentrations above 6.5 mmol/l which is 250 mg/dl. There were significant sex differences in a number of risk factors with males having significantly higher prevalence of low high density lipoprotein, systolic and diastolic blood pressures, obesity, and smoking than women. About 8% of men and women were obese (as defined by a body mass index > 30), while 47% of men and 35% of women were mildly overweight (body mass index > 25). Two or more risk factors for coronary heart disease (high total cholesterol and/or hypertension and/or obesity) were present in 4% and 9% of older men and women respectively. Furthermore, about half the subjects had more than one risk factor for coronary heart disease.     

Atorvastatin increases human serum levels of proprotein convertase subtilisin/kexin type 9

Proprotein convertase subtilisin/kexin type 9 (PCSK9) has gained attention as a key regulator of serum low density lipoprotein cholesterol (LDL-C) levels. This novel protease causes the degradation of hepatic low density lipoprotein receptors. In humans, gain-of-function mutations in PCSK9 cause a form of familial hypercholesterolemia, whereas loss-of-function mutations result in significantly decreased LDL-C levels and cardiovascular risk. Previous studies have demonstrated that statins upregulate PCSK9 mRNA expression in cultured cells and animal models. In light of these observations, we studied the effect of atorvastatin on circulating PCSK9 protein levels in humans using a sandwich ELISA to quantitate serum PCSK9 levels in patients treated with atorvastatin or placebo for 16 weeks. We observed that atorvastatin (40 mg/day) significantly increased circulating PCSK9 levels by 34% compared with baseline and placebo and decreased LDL-C levels by 42%. These results suggest that the addition of a PCSK9 inhibitor to statin therapy may result in even further LDL-C decreases.     

An apolipoprotein A-I mimetic dose-dependently increases the formation of prebeta1 HDL in human plasma

Prebeta1 HDL is the initial plasma acceptor of cell-derived cholesterol in reverse cholesterol transport. Recently, small amphipathic peptides composed of D-amino acids have been shown to mimic apolipoprotein A-I (apoA-I) as a precursor for HDL formation. ApoA-I mimetic peptides have been proposed to stimulate the formation of prebeta1 HDL and increase reverse cholesterol transport in apoE-null mice. The existence of a monoclonal antibody (MAb 55201) and a corresponding ELISA method that is selective for the detection of the prebeta(1) subclass of HDL provides a means of establishing a correlation between apoA-I mimetic dose and prebeta1 HDL formation in human plasma. Using this prebeta1 HDL ELISA, we demonstrate marked apoA-I mimetic dose-dependent prebeta1 HDL formation in human plasma. These results correlated with increases in band density of the plasma prebeta1 HDL, when observed by Western blotting, as a function of increased apoA-I mimetic concentration. Increased prebeta1 HDL formation was observed after as little as 1 min and was maximal within 1 h. Together, these data suggest that a high-throughput prebeta1 HDL ELISA provides a way to quantitatively measure a key component of the reverse cholesterol transport pathway in human plasma, thus providing a possible method for the identification of apoA-I mimetic molecules.     

Structural and functional consequences of the Milano mutation (R173C) in human apolipoprotein A-I

Carriers of the apolipoprotein A-I_Milano (apoA-I_M) variant, R173C, have reduced levels of plasma HDL but no increase in cardiovascular disease. Despite intensive study, it is not clear whether the removal of the arginine or the introduction of the cysteine is responsible for this altered functionality. We investigated this question using two engineered variations of the apoA-I_M mutation: R173S apoA-I, similar to apoA-I_M but incapable of forming a disulfide bond, and R173K apoA-I, a conservative mutation. Characterization of the lipid-free proteins showed that the order of stability was wild type≈R173K>R173S>R173C. Compared with wild-type apoA-I, apoA-I_M had a lower affinity for lipids, while R173S apoA-I displayed intermediate affinity. The in vivo effects of the apoA-I variants were measured by injecting apoA-I-expressing adeno-associated virus into apoA-I-null mice. Mice that expressed the R173S variant again showed an intermediate phenotype. Thus, both the loss of the arginine and its replacement by a cysteine contribute to the altered properties of apoA-I_M. The arginine is potentially involved in an intrahelical salt bridge with E169 that is disrupted by the loss of the positively charged arginine and repelled by the cysteine, destabilizing the helix bundle domain in the apoA-I molecule and modifying its lipid binding characteristics.     

Homeostasis of free cholesterol in the blood: a preliminary evaluation and modeling of its passive transport

The rate of noncatalyzed transfer of cholesterol (Chol) among lipoproteins and cells in the blood is of fundamental importance as a baseline to assess the role of active transport mechanisms, but remains unknown. Here we address this gap by characterizing the associa­tion of the Chol analog, ergosta-5,7,9(11),22-tetraen-3β-ol (DHE), with the lipoproteins VLDL, LDL, HDL₂, and HDL₃. Combining these results with data for the association of DHE with liposomes, we elaborated a kinetic model for the noncatalyzed exchange of free Chol among blood compartments. The computational results are in good agreement with experimental values. The small deviations are explained by the nonequilibrium distribution of unesterified Chol in vivo, due to esterification and entry of new unesterified Chol, and eventual effects introduced by incubations at low temperatures. The kinetic profile of the homeostasis of unesterified Chol in the blood predicted by the model developed in this work is in good agreement with the observations in vivo, highlighting the importance of passive processes.     

Lecithin:cholesterol acyltransferase: old friend or foe in atherosclerosis?

Lecithin:cholesterol acyltransferase (LCAT) is a key enzyme that catalyzes the esterification of free cholesterol in plasma lipoproteins and plays a critical role in high-density lipoprotein (HDL) metabolism. Deficiency leads to accumulation of nascent preβ-HDL due to impaired maturation of HDL particles, whereas enhanced expression is associated with the formation of large, apoE-rich HDL(1) particles. In addition to its function in HDL metabolism, LCAT was believed to be an important driving force behind macrophage reverse cholesterol transport (RCT) and, therefore, has been a subject of great interest in cardiovascular research since its discovery in 1962. Although half a century has passed, the importance of LCAT for atheroprotection is still under intense debate. This review provides a comprehensive overview of the insights that have been gained in the past 50 years on the biochemistry of LCAT, the role of LCAT in lipoprotein metabolism and the pathogenesis of atherosclerosis in animal models, and its impact on cardiovascular disease in humans.     

Levels of atherogenic lipoproteins are unexpectedly reduced in interstitial fluid from type 2 diabetes patients

At a given level of serum cholesterol, patients with T2D have an increased risk of developing atherosclerosis compared with nondiabetic subjects. We hypothesized that T2D patients have an increased interstitial fluid (IF)-to-serum gradient ratio for LDL, due to leakage over the vascular wall. Therefore, lipoprotein profiles in serum and IF from 35 T2D patients and 35 healthy controls were assayed using fast performance liquid chromatography. The IF-to-serum gradients for VLDL and LDL cholesterol, as well as for apoB, were clearly reduced in T2D patients compared with healthy controls. No such differences were observed for HDL cholesterol. Contrary to our hypothesis, the atherogenic VLDL and LDL particles were not increased in IF from diabetic patients. Instead, they were relatively sparser than in healthy controls. The most probable explanation to our unexpected finding is that these lipoproteins are more susceptible to retainment in the extravascular space of these patients, reflecting a more active uptake by, or adhesion to, tissue cells, including macrophages in the vascular wall. Further studies are warranted to further characterize the mechanisms underlying these observations, which may be highly relevant for the understanding of why the propensity to develop atherosclerosis is increased in T2D.