低密度脂蛋白和氧化型低密度脂蛋白对HepG2细胞肝脂酶活性及肝脂酶mRNA表达的影响

为观察低密度脂蛋白和氧化型低密度脂蛋白对肝脂酶合成和肝脂酶活性的影响 ,将不同浓度的低密度脂蛋白、氧化型低密度脂蛋白与人肝癌细胞株HepG2细胞共同培养 ,用MTT法测定细胞增殖抑制率 ,用组织化学法测定细胞肝脂酶活性 ,用逆转录聚合酶链反应测定细胞肝脂酶mRNA的表达水平。结果发现 ,低密度脂蛋白浓度在 2 7.4 7、5 4 .95mg/L时HepG2细胞逆转录聚合酶链反应产物的吸光度值分别是细胞对照的 2 .8倍和 2 .3倍 ,浓度在 10 9.89mg/L时逆转录聚合酶链反应产物的吸光度值与细胞对照比较降低 2 0 %。细胞肝脂酶活性随低密度脂蛋白浓度增加而降低 ,两者呈负相关 (r=- 0 .95 6 14 ,P <0 .0 5 ) ;低密度脂蛋白浓度在 5 4 .95mg/L时开始产生细胞增殖抑制作用 ,其细胞增殖抑制率与低密度脂蛋白浓度呈正相关 (r=0 .91199,P <0 .0 5 )。不同浓度的氧化型低密度脂蛋白处理HepG2细胞其肝脂酶mRNA逆转录聚合酶链反应产物的吸光度值均低于细胞对照孔 ;脂蛋白浓度为2 7.4 7、5 4 .95及 10 9.89mg/L时低密度脂蛋白组细胞肝脂酶活性是氧化型低密度脂蛋白组的 3～ 4倍 ;浓度在 5 4 .95mg/L时氧化型低密度脂蛋白对细胞的增殖抑制作用是低密度脂蛋白的 2倍。结果提示 ,低密度脂蛋白在一定浓度范围能诱导HepG2细胞肝脂酶mRNA     

溃疡性结肠炎患者外周血单个核细胞中Foxp3 mRNA的表达水平

目的:探讨溃疡性结肠炎(UC)患者外周血单个核细胞中Foxp3 mRNA表达及其与疾病活动性的关系．方法:应用逆转录-聚合酶链反应(RT-PCR) 检测142例UC患者(活动期22例、缓解期20例) 和30例正常对照组外周血单个核细胞Foxp3 mRNA的表达水平．结果:UC患者急性期Foxp3 mRNA水平低于正常人,差异有显著性(1．58±0．31 vs 3．27± 0．40,P<0．05);缓解期Foxp3 mRNA水平与正常人差异无显著性(P=0．104);PBMC中Foxp3 mRNA表达水平与Walmsley评分标准有相关性,且呈负相关．结论:UC患者外周血单个核细胞中Foxp3 mRNA表达水平显著低于正常人,其参与了 UC的发病过程并与疾病的活动性有关．     

中国人内源性高甘油三酯血症与脂蛋白脂酶基因HindⅢ多态性的关系

为了解中国人内源性高甘油三酯血症与脂蛋白脂酶基因多态性是否相关,用聚合酶链反应－限制片长多态性方法对成都地区200例内源性高甘油三酯血症患者及220例血脂正常者脂蛋白脂酶基因HindⅢ酶切位点的多态性及其血脂、载脂蛋白水平进行了研究。结果发现,内源性高甘油三酯血症患者和正常人均以H2H2纯合于基因型为主,内源性高甘油三酯血症组H2等位基因频率较对照组增加（0．855比0．745,P＜0．01）;而H1等位基因频率内源性高甘油三酯血症组则明显低于对照组（0．145比0．255,P＜0．01）。H2H2基因型者血浆甘油三脂、载脂蛋白CⅡ、CⅢ水平、甘油三酯与高密度脂蛋白的比值均显著高于H1H1基因型者（P＜0．01）,比H1H2基因型者有明显增加（P＜0．05）。此结果显示,脂蛋白脂酶基因内含子HindⅢ酶切位点的多态性与中国人内源性高甘油三酯血症有一定的相关性。     

三磷酸腺苷结合盒转运体A1在糖尿病小型猪组织中表达的变化

用贵州小香猪建立 2型糖尿病动物模型 ,探讨糖尿病小型猪三磷酸腺苷结合盒转运体A1表达的变化。采用高脂高蔗糖饲料喂养贵州小香猪 ,建立 2型糖尿病动物模型。血浆总胆固醇、甘油三酯、高密度脂蛋白胆固醇和葡萄糖的浓度均用氧化酶法测定 ,血浆游离脂肪酸用比色法测定 ,采用逆转录—聚合酶链反应、Western印迹和免疫组织化学法分别检测三磷酸腺苷结合盒转运体A1mRNA和蛋白质的表达。喂养 6个月后 ,实验组与正常对照组比较 ,空腹血糖值明显升高 ;空腹胰岛素水平在头 3个月轻度升高 ,在第 6个月末其水平降低 ;血清总胆固醇、甘油三酯和游离脂肪酸水平升高。采用逆转录—聚合酶链反应检测组织细胞三磷酸腺苷结合盒转运体A1mRNA的表达 ,结果显示 ,与对照组小型猪比较 ,实验组小型猪肝组织、冠状动脉和肾组织三磷酸腺苷结合盒转运体A1mRNA表达上调 (P <0 .0 5 )。Westernblot检则肝组织、冠状动脉和肾组织三磷酸腺苷结合盒转运体A1蛋白质的表达 ,结果显示 ,与对照组小型猪比较 ,高脂高蔗糖饲料喂养的小型猪肝组织、冠状动脉和肾组织三磷酸腺苷结合盒转运体A1蛋白质表达明显增高 (P <0 .0 5 )。免疫组织化学检测的结果与Westernblot检则结果相一致 ,实验组小型猪肝组织、冠状动脉和肾组织切片上棕褐色或棕黄色     

天然及氧化型极低密度脂蛋白诱导培养的人脐静脉内皮细胞表达巨噬细胞炎性蛋白1α

为探讨天然及氧化型极低密度脂蛋白能否诱导培养的人脐静脉内皮细胞表达巨噬细胞炎性蛋白 1α ,使内皮细胞分别暴露于上述脂蛋白后 ,用原位杂交、逆转录聚合酶链反应及免疫细胞化学法分别检测各组细胞的巨噬细胞炎性蛋白 1αmRNA和蛋白的表达。原位杂交发现 ,培养的内皮细胞能表达巨噬细胞炎性蛋白 1αmRNA ,两脂蛋白组内皮细胞的积分吸光度值明显高于对照组 (P <0 .0 1)。逆转录聚合酶链反应发现 ,两脂蛋白组内皮细胞的巨噬细胞炎性蛋白 1αmRNA的积分吸光度值分别为对照组的 15 .4倍和 14 .2倍。免疫细胞化学发现 ,两脂蛋白组内皮细胞胞浆的巨噬细胞炎性蛋白 1α蛋白表达 (棕色颗粒 )的积分吸光度值显著高于对照组 ,方差分析表明 ,组间差异有显著性意义 (P <0 .0 5 )。结果提示 ,天然及氧化型极低密度脂蛋白均可诱导培养的人脐静脉内皮细胞表达高水平的巨噬细胞炎性蛋白 1αmRNA和蛋白 ,通过促进单核细胞迁入内膜在动脉粥样硬化发生中起重要作用     

外周血核转录因子过氧化物酶体增殖物激活受体γmRNA与脂连素水平和冠状动脉病变严重程度的相关性分析研究

目的:研究外周血核转录因子过氧化物酶体增殖物激活受体γ(PPARγ)mRNA表达与血清脂连素浓度和冠状动脉(冠脉)病变严重程度的相关性.方法:经冠脉造影检查后将142例患者分为冠心病组(经造影确诊冠心病者107例)和对照组(经造影排除冠心病者35例).逆转录多聚合酶链反应法测定外周血细胞中PPARγmRNA表达,酶联免疫吸附剂(ELISA)法检测血清中脂连素含量;并根据造影结果对冠脉病变进行Gensini评分,分析PPARγ mRNA、脂连素水平与冠脉病变Gensini评分的相关性.结果:冠心病组PPARγ和脂连素水平较对照组明显降低,差异具统计学意义(P均<0.05).PPARγ mRNA及脂连素与冠脉病变Gensini评分呈负相关关系(r=-0.898,r=-0.923,P均<0.05),PPARγ mRNA表达和脂连素水平呈明显正相关关系(r=0.875,P<0.05).结论:PPARγ和脂连素是冠脉粥样硬化的负调控因子,对冠心病高危人群具有保护作用.     

急性心肌梗死大鼠心脏一氧化氮合酶表达的改变

目的 通过建立大鼠心肌梗死模型，观察急性心肌梗死对大鼠心脏内皮型一氧化氮合酶mRNA和诱导型一氧化氮合酶蛋白表达的影响。方法48只健康成年SD大鼠（体重200～250g）随机分为假手术组和缺血组，取1、2、8和24h四个不同时间点观察。采用开胸结扎冠状动脉左前降支建立心肌缺血模型，逆转录聚合酶链反应检测大鼠心肌梗死后1、2及24h三个时段缺血心肌内皮型一氧化氮合酶mRNA的表达；免疫组织化学染色检测冠状动脉结扎后8h缺血心肌诱导型一氧化氮合酶蛋白的表达。结果冠状动脉结扎后2h，缺血组大鼠缺血心肌组织内皮型一氧化氮合酶mRNA表达下降（P〈0．05），并持续至结扎后24h；结扎后24h组内皮型一氧化氮mRNA的表达与结扎后2h组相比无显著性差异（P〉0．05）。冠状动脉结扎后8h，梗死区存活心肌组织细胞诱导型一氧化氮合酶蛋白大量表达，而假手术组未见诱导型一氧化氮合酶蛋白表达。结论正常大鼠心肌组织有内皮型一氧化氮合酶基因表达，无诱导型一氧化氮合酶蛋白表达。在心肌梗死早期缺血心肌内皮型一氧化氮合酶mRNA表达减少。心肌急性缺血刺激早期诱导大鼠缺血心肌组织诱导型一氧化氮合酶蛋白大量表达。     

脂联素基因SNP-11377多态性与冠脉病变程度相关性研究

目的探讨在中国上海地区汉族人群中脂联素基因（APM1）启动子序列单核苷酸多态性（SNP）与冠脉病变程度的关系。方法采用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）方法，分析了325例冠脉造影结果和脂联素启动子序列单核苷酸多态性（-11377G／C）的关系．研究设立了冠心病组（CAD）和正常对照组，并根据冠脉造影结果按照不同病变支数及Gensini评分将分成不同病变组，分析-11377位点基因型及基因频率的差异性。结果（1）冠心病组脂联素基因-11377位点多态性GC、GG基因型频率与对照组比较，显著高于对照组，差异有极显著性（χ^2=12．619，P〈0．05）；（2）冠心病患者脂联素-11377位点G等位基因频率显著高于正常人（χ^2=11．291，P〈0．05）；（3）根据冠脉造影结果冠脉不同病变支数各组比较，脂联素-11377位点基因型差异无显著性（χ^2=11．575，P〉0．05），而等位基因频率具有显著差异性（χ^2=11．582，P〈0．05）；（4）按Genisini标准冠状动脉不同积分各组之间比较脂联素基因型间差异无显著性（χ^2=10．983，P〉0．05），但等位基因频率具有显著差异性（χ^2=8．978，P〈0．05）。结论脂联素SNP-11377G／C各种基因型与冠心病有关，与冠状动脉粥样硬化病变程度无关，而等位基因频率不但与冠心病显著相关，并且与冠状动脉病变程度有关。     

缬沙坦对兔主动脉PPAR-γmRMA及其蛋白表达的影响

目的研究缬沙坦对兔主动脉过氧化物酶体增殖物激活受体-γ（PPAR-γ）表达的影响，探讨其抗动脉硬化（AS）的可能机制。方法将24只新西兰兔随机分成正常对照组、高脂组、药物组，分别给予正常饮食、高脂饮食、高脂饮食加缬沙坦灌胃，共14周。采用逆转录聚合酶链反应及免疫组化法分别检测兔主动脉PPAR-γ mRNA及其蛋白表达，并测量主动脉内膜厚度及内膜／中膜厚度比。结果药物组内膜厚度低于高脂组（P〈0．05）。主动脉PPAR-γ表达药物组〉高脂组〉对照组．P均〈0．05。药物组主动脉PPAR-γ蛋白表达高于高脂组（P〈0．05）．对照组未见明显表达。结论缬沙坦可能通过增加PPAR-γ表达而发挥抗AS作用。     

脂蛋白脂酶S447X和胆固醇酯转运蛋白TaqIB基因多态性与冠心病的关系

目的　探讨脂蛋白脂酶 (LPL)基因S4 4 7X和胆固醇酯转运蛋白 (CETP)TaqIB与冠心病的关系。方法　对 2 4 9例经冠状动脉造影证实为冠心病的患者及 16 7例经冠状动脉造影证实无冠状动脉病变的对照者进行研究 ,采用酶法测定血脂各项水平 ,采用多聚酶链反应 限制性内切酶片段长度多态性 (PCR RFLP)分析LPL基因中S4 4 7X及CETP基因中TaqIB的基因多态性。 结果　冠心病组与对照组比较 ,LPLS4 4 7X和CETPTaqIB基因型与等位基因频率分布无显著性差异 ,P >0 0 5。甘油三酯≥ 1 7mmol/L时 ,B2 B2 组高密度脂蛋白胆固醇水平升高 ,P <0 0 5。甘油三酯 <1 7mmol/L时 ,SX/XX组血脂各项与SS组比较均有显著性差异 ,P <0 0 5 ;B2 B2 组高密度脂蛋白胆固醇水平升高 ,P <0 0 5。在B1B1基因型中 ,当S突变为X时 ,血浆总胆固醇和甘油三酯水平明显降低 ,P <0 0 5 ;在B1B2 基因型中 ,当S突变为X时 ,血浆总胆固醇和低密度脂蛋白胆固醇水平下降 ,P<0 0 5 ;在B2 B2 基因型中 ,当S突变为X时 ,血浆高密度脂蛋白胆固醇水平明显升高 ,P <0 0 1。结论　S、X、B1、B2 等位基因频率的分布在冠心病组及对照组之间无明显差异     

Lipoprotein (A) in patients with coronary atherosclerosis]

The serum level of lipoprotein (a) (LP(a] was measured in 117 patients with coronary heart disease (CHD) angiographically documented, 22 patients with unaltered coronary arteries as evidenced by coronary angiography (Control Group 1), and 28 subjects without clinical CHD signs (Control Group 2). Total cholesterol, triglycerides, low and high density lipoprotein cholesterol, and apolipoproteins (apo) AI and B were measured in the patients and healthy subjects. They were found to be higher in CHD patients than in patients with unaltered arteries and healthy subjects. The level of LP(a) was significantly increased in patients with three-vessel disease as compared to the control groups and patients with single-vessel disease. There was no relation of LP(a) to total cholesterol, triglyceride, high density lipoprotein cholesterol, low and very low density lipoprotein cholesterol, apo-AI, apo-B, age, and sex. The findings supports the assumption that LP(a) is associated with coronary atherosclerosis.     

Higher level of plasma cholesteryl ester transfer activity from high-density lipoprotein to Apo B-containing lipoproteins in subjects with angiographically detectable coronary artery disease

Background and hypothesis: Plasma high-density lipoprotein cholesterol (HDL-C) levels correlate inversely with the incidence of coronary artery disease. In order to ascertain whether the transfer activity is related to coronary atherosclerosis, we studied plasma cholesteryl ester transfer activity (CETA) from HDL to apo B-containing lipoproteins in a consecutive series of 64 Japanese men aged <60 years who had undergone diagnostic coronary angiography. Methods: The subjects were divided into two groups: those who had ≥50% luminal stenosis in one or more coronary arteries (Group 1) and those who had <50% stenosis (Group 2). Results: CETA was 20.8±6.0%/2h in 38 subjects in Group 1. significantly higher than 17.4±6.9%/2h in 26 subjects in Group 2(p<0.05). Plasma HDL-C levels in Group 1 were significantly lower than those in Group 2(p<0.05). CETA correlated inversely with HDL-C levels (r = ?0.46, p<0.001). Plasma total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and Lp(a) levels did not differ significantly between the two groups. There was no significant correlation between CETA and either LDL-C or TG levels. Conclusion: Results suggest that high CETA is realted to low plasma HDL-C levels and may lead to the development of coronary atherosclerosis. Also, CETA was independent of plasma LDL-C or TG levels.     

老年冠心病患者血浆非高密度脂蛋白胆固醇水平的差异

目的探讨在老年冠心病患者的血清非高密度脂蛋白胆固醇的差异。方法选择120例行冠状动脉造影检查的老年患者,冠状动脉造影前空腹采静脉血,分析冠状动脉造影阳性组和对照组之间非高密度脂蛋白胆固醇与其它血脂数据(总胆固醇、甘油三酯、高密度脂蛋白、低密度脂蛋白)差异的显著性及非高密度脂蛋白胆固醇对冠状动脉病变程度的相关性。结果冠状动脉造影阳性组非高密度脂蛋白胆固醇水平显著高于阴性组2.99±1.08mmol/L,一支病变组为3.41±0.59mmol/L,两支病变组为3.70±1.30mmol/L,三支病变组为3.77±1.10mmol/L,(P<0.001)并且非高密度脂蛋白的水平随冠状动脉病变支数逐渐增高,与冠状动脉狭窄分数相关(r=0.36,P<0.001);而两组间甘油三酯,高密度脂蛋白水平无统计学差异(P>0.05)。结论血清非高密度脂蛋白胆固醇对于老年人是一项简便实用的冠心病风险评估指标。     

Preheparin serum lipoprotein lipase mass is negatively related to coronary atherosclerosis

In preheparin serum, there exists lipoprotein lipase (LPL) mass with little activity. The clinical significance of this preheparin serum LPL mass (preheparin LPL mass) is unclear. We studied the levels of preheparin LPL mass in patients with coronary atherosclerosis, comparing the results with those in healthy men. We also evaluated the correlation between preheparin LPL mass and the severity of coronary atherosclerosis by comparing with other risk factors such as age, smoking, family history, hypertension, hyperuricemia, diabetes mellitus, total cholesterol, triglyceride, high density lipoprotein-cholesterol and body mass index. The subjects, 70 men presenting with symptoms of coronary artery disease, underwent coronary angiographic examination. Significant narrowness was defined as > or = 75%. Control group comprised 77 men who had annual health checks and showed no abnormal findings. Preheparin LPL mass in the stenosis group was lower than normal coronary group and also than the control group. Multivariate analysis showed that preheparin LPL mass had the highest t-value (-2.53) for the number of lesions among the risk factors listed above. These results suggest that low preheparin LPL mass may be deeply involved in the progression of coronary atherosclerosis.     

Alcohol consumption, serum lipids and severity of angiographically determined coronary artery disease

The relation of alcohol consumption to serum lipids and the severity of coronary atherosclerosis was examined in 212 men undergoing coronary angiography. The severity of coronary atherosclerosis was assessed in terms of the presence of greater than or equal to 75% diameter stenosis and the Gensini severity score. Alcohol consumption was divided into 4 categories: none (0 ml alcohol/week), light (1 to 100 ml alcohol/week), moderate (101 to 300 ml alcohol/week) and heavy (greater than or equal to 301 ml alcohol/week). Alcohol consumption was positively related to high-density lipoprotein cholesterol and inversely related to total cholesterol, but was not associated with triglyceride. After adjustment for these serum lipids as well as for cigarette smoking and systemic hypertension, the risk of coronary stenosis was significantly decreased in the moderate drinkers. A decreased risk among moderate drinkers also was noted in terms of Gensini's severity score. These findings suggest that moderate alcohol consumption may protect against severe coronary atherosclerosis.     

Expression of fat mobilizing genes in human epicardial adipose tissue

BackgroundEpicardial adipose tissue (EAT) mass correlates with Metabolic Syndrome and coronary artery disease (CAD). However, little is known about the expression of genes involved in triglyceride (TG) storage and mobilization in EAT. We therefore analyzed the expression of genes involved in fat mobilization in EAT in comparison to subcutaneous abdominal adipose tissue (AAT) in CAD patients and in controls.MethodsEAT and AAT were obtained during coronary artery bypass graft (CABG) surgery from 16 CAD patients and from 14 non-CAD patients presenting for valve surgery. The state of atherosclerosis was assessed by angiography. RNA from tissues were extracted, reversibly transcribed and quantified by real time polymerase chain reaction (RT-PCR). The following genes were analyzed: perilipin-1 and -5 (PLIN1, PLIN5), lipoprotein lipase (LPL), hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL), comparative gene identification-58 (CIG-58), angiopoietin like protein 4 (ANGPTL4), in addition to interleukine-6 (IL-6), leptin (LEP) and adiponectin (ADPN).ResultsA significant expression of all listed genes could be observed in EAT. The relative expression pattern of the 10 genes in EAT was comparable to the expression in AAT, yet there was a significantly higher overall expression in AAT. The expression of the listed genes was not different between CAD patients and controls.ConclusionIt is suggested that the postulated difference in EAT volume between CAD patients and non-CAD patients is not caused by a differential mRNA expression of fat mobilizing genes. Further work on protein levels and enzyme activities will be necessary to get a complete picture.     

Relationships of low density lipoprotein subfractions to angiographically defined coronary artery disease in young survivors of myocardial infarction.

Low density lipoprotein (LDL) from 36 young post-infarction patients was separated by isopycnic density gradient ultracentrifugation to determine the relationships of plasma levels and chemical composition of different LDL subfractions to the global severity and rate of progression of coronary atherosclerosis assessed by angiography. There were marked elevations of the cholesterol and triglyceride concentrations in the very low density lipoprotein (VLDL) fraction, whereas the high density lipoprotein (HDL) cholesterol level was reduced in the patients compared with 70 healthy population-based controls. Plasma total LDL cholesterol and triglyceride concentrations were similar. The distribution of apolipoprotein B along the LDL density range, viz. the LDL particle distribution, was displaced towards the dense LDL region among the patients compared with 14 healthy normolipidaemic controls. A preponderance of dense LDL particles was associated with elevated plasma VLDL triglyceride concentration. The patients had significantly higher plasma concentrations of lipid and protein in dense LDL (d greater than 1.040 kg/l), while no group differences were found in the light LDL (d less than 1.040 kg/l). However, there were no percentage compositional differences in the light or dense LDL between patients and controls. Among all constituents of lipoprotein fractions and subfractions determined, only the plasma level of triglycerides in both light and dense LDL correlated significantly with the angiographic estimates of global severity and rate of progression of coronary atherosclerosis, respectively. On a percentage composition basis, both light and dense LDL tended to be richer in triglycerides in the subjects with a more severe coronary artery disease. Neither VLDL or HDL, nor LDL cholesterol were associated with the angiographic scores, the plasma LDL triglyceride concentration or the triglyceride enrichment of LDL. Although there is ample experimental evidence that triglyceride-enriched LDL predisposes to atherosclerosis, the LDL associations with coronary lesion severity and progression observed in the present study might not reflect a causal mechanism, but merely mirror the atherogenicity of disturbances affecting the metabolism of triglyceride-rich lipoproteins. Prospective studies of larger groups of unselected patients are needed to corroborate these findings.     

金花茶对衰老大鼠脂代谢及肝细胞凋亡的影响

目的 探讨金花茶调节衰老大鼠脂代谢及抗肝凋亡的作用.方法 健康雄性SD大鼠40只随机分为4组.1组为空白对照组,2～4组予D-半乳糖腹腔注射法建立大鼠亚急性衰老模型后,其中2组作为衰老模型组,3、4组再分别以高、低浓度金花茶灌胃干预40天.测大鼠尾静脉血总胆固醇、甘油三酯、高密度脂蛋白和低密度脂蛋白含量,测肝脏组织总胆固醇、甘油三酯含量和Bcl-2、Bax mRNA表达水平.结果 与衰老模型组相比,高、低浓度金花茶干预组大鼠血清高密度脂蛋白浓度和Bcl-2 mRNA显著升高(P＜0.05);血清总胆固醇、甘油三酯、低密度脂蛋白浓度和肝组织总胆固醇、甘油三酯含量、Bax mRNA表达水平显著降低(P＜0.05).高、低浓度金花茶组间比较,上述指标有统计学差异(P＜0.05).结论 金花茶可调节衰老大鼠的血脂,减少肝脏脂肪堆积,降低肝细胞凋亡水平,以降低动脉粥样硬化发病风险.     

Postprandial adipose tissue lipoprotein lipase activity in primary hypertriglyceridemia

The fasting activity of adipose tissue lipoprotein lipase has been previously reported to be either normal or reduced in subjects with a primary form of hypertriglyceridemia. The postprandial activity of adipose tissue lipoprotein lipase has not been previously reported in these subjects. In subjects with primary hypertriglyceridemia the fasting lipoprotein lipase activity eluted from pieces of adipose tissue by heparin and the enzyme activity present in extracts of acetone-ether tissue powders were similar to the level of enzyme activity found in normal subjects. There also was no difference in the postprandial adipose tissue heparin-elutable lipoprotein lipase activity between these two groups when measured after high carbohydrate feeding. When the subjects with primary hypertriglyceridemia were further subdivided by genetic diagnosis, there was no difference in the level of adipose tissue lipoprotein lipase of subjects with familial hypertriglyceridemia, familial combined hyperlipidemia, or in those in whom no specific genetic diagnosis could be made. The change in lipoprotein lipase activity after feeding was inversely related to the fasting enzyme level in both the normal subjects (r = ?0.58, p < 0.05, n = 12) and the hypertriglyceridemic subjects (r = ?0.92, p < 0.01, n = 11). In the normal subjects, the plasma triglyceride response to feeding correlated inversely with the postprandial change in lipoprotein lipase activity (r = ?0.76, p < 0.02, n = 12). Adipose tissue lipoprotein lipase activity in patients with primary lipoprotein lipase deficiency was markedly reduced in the fasting state and remained essentially zero after feeding. This suggests that a functional role exists for the enzyme activity as measured.     

Lipoprotein alterations in hemodialysis: differences between diabetic and nondiabetic patients

Both renal failure and type 2 diabetes may contribute synergistically to the dyslipemia of diabetic renal failure with the development of atherosclerosis as the possible consequence. It has not yet been conclusively evaluated whether diabetic patients with end-stage renal failure under maintenance hemodialysis (HD) show accentuated alterations in plasma lipids and lipoproteins in comparison to nondiabetics under HD. These abnormalities would involve hepatic lipase activity and the regulation of triglyceride-rich lipoprotein metabolism. The purpose of the present study was to evaluate whether type 2 diabetic patients undergoing HD exhibited a lipid-lipoprotein profile different from that of nondiabetic hemodialyzed patients. We compared plasma lipids, apoprotein (apo) A-I and B, and lipoprotein parameters among 3 groups: 25 type 2 diabetics, 25 nondiabetics, both undergoing HD, and 20 healthy control subjects. Intermediate-density lipoprotein (IDL) and low-density lipoprotein (LDL) were isolated by sequential ultracentrifugation. Hepatic lipase activity was measured in postheparin plasma. Both groups of HD patients showed higher triglyceride and IDL cholesterol (P <.001), and lower high-density lipoprotein (HDL) cholesterol (P <.01) and apo A-I (P <.001) levels compared to the control group, even after adjustment for age and body mass index (BMI). However, no differences were found in lipid, lipoprotein, and apoprotein concentrations between diabetic and nondiabetic HD patients, except for high LDL triglyceride content of diabetic HD patients (P <.01). Nondiabetics undergoing HD also presented higher LDL triglyceride levels than controls (P <.05). LDL triglyceride correlated with plasma triglycerides (r = 0.51, P <.001). A lower LDL cholesterol/apo B ratio was found in each group of HD patients in comparison to controls (P <.02). Comparing the diabetic and nondiabetic patients, hepatic lipase activity remained unchanged, but significantly lower than control subjects (P <.001). Hepatic lipase correlated with log-triglyceride (r = -0.31, P <.01), IDL cholesterol (r = -0.41, P <.001), and LDL triglyceride (r = -0.32, P <.01). In conclusion, both diabetic and nondiabetic HD patients shared unfavorable alterations in lipid-lipoprotein profile not different between them but different from a healthy control group. The only difference between the groups of HD patients was a significant LDL triglyceride enrichment, which correlated negatively with hepatic lipase activity. Lipoprotein abnormalities in HD patients would enhance their risk for the development of atherosclerosis.