正常人餐后甘油三酯动态代谢对血清一氧化氮和血浆内皮素1的影响

为探讨正常人脂肪负荷后甘油三酯动态代谢对血清一氧化氮和血浆内皮素 1浓度的影响 ,取 2 0例正常人标准脂肪餐前 (0h)、餐后 2、4、6和 8h外周静脉血 ,分离血清 ,测定甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、载脂蛋白AⅠ和载脂蛋白B水平 ,放射免疫法测定血浆内皮素 1浓度 ,比色法测定血清一氧化氮相对浓度 ,计算一氧化氮 /内皮素 1比值。结果发现 ,餐后 2h血清甘油三酯浓度显著高于餐前 (2 .19± 0 .16比 1.161.16± 0 .11mmol/L ,P <0 .0 5 ) ,4h达到高峰 (3.34± 0 .37mmol/L) ,8h恢复至餐前水平。餐后 2h血浆一氧化氮浓度存在一过性升高 (61.5 8± 5 .97比 42 .5 0± 7.42ng/L ,P <0 .0 5 ) ,6、8h又显著降低 (37.60± 5 .71比 61.5 8± 5 .97ng/L ;30 .76± 5 .0 1比 61.5 8± 5 .97ng/L ,P <0 .0 5 )。餐后 2h内皮素 1浓度较餐前显著降低(99.0 8± 16.5 5比 114.2 2± 16 .45ng/L ,P <0 .0 5 ) ,餐后 6、8h较 2h显著升高 (113.82± 19.80比 99.0 8± 16 .5 5ng/L ,12 1.0 2± 19.5 5比 99.0 8± 16.5 5ng/L ,P <0 .0 5 ) ,餐后 8h较 4h高 (12 1.0 2± 19.5 5比 10 3.45± 19.87ng/L ,P <0 .0 5 )。同样 ,一氧化氮 /内皮素 1比值在餐后 2h存在高峰 (0 .78± 0 .13比 0 .46±     

原发性高血压患者脂餐后甘油三酯代谢异常与颈动脉内中膜复合体厚度的关系

为探讨原发性高血压患者是否存在脂肪负荷后血清富含甘油三酯脂蛋白代谢异常及其与颈动脉内中膜复合体厚度之间的关系 ,选择 38例原发性高血压患者和 30例健康人 (对照组 ) ,禁食 10～ 12h后 ,采用二维血管超声测定双侧颈动脉内中膜复合体厚度。随后进行标准脂肪负荷试验 ,分别以甘油三酯 8h曲线下面积和甘油三酯峰反应作为脂肪负荷后甘油三酯反应水平的指标。发现 :①原发性高血压组甘油三酯峰反应 (4.6 8± 1.74mmol L比 1.76± 0 .6 4mmol L)及甘油三酯曲线下面积 (2 3.5 9± 6 .4 8mmol L比 9.5 6± 3.38mmol L ,8h)显著大于对照组 (P<0 .0 5 ) ;②原发性高血压组颈动脉内中膜复合体厚度显著大于对照组 (0 .76 7± 0 .15mm比 0 .6 0 3± 0 .0 5mm ,P <0 .0 1) ;③原发性高血压患者的颈动脉内中膜复合体厚度与甘油三酯曲线下面积、年龄、甘油三酯峰反应、肥胖指数呈正相关 (r=0 .4 97、0 .4 4 8、0 .382、0 .35 2 ,P <0 .0 5 ) ,同空腹高密度脂蛋白水平呈负相关 (r =- 0 .2 87,P =0 .0 0 2 )。提示原发性高血压患者存在脂餐后甘油三酯代谢异常 ,高血压和餐后甘油三酯代谢异常均与颈动脉内中膜复合体厚度的增加有关。     

肥胖和高血压患者餐后甘油三酯代谢异常与胰岛素抵抗的关系

目的　探讨高血压病与肥胖患者餐后甘油三酯 (TG)代谢异常与胰岛素抵抗的关系。方法　 19例健康人 ,19例单纯肥胖患者 ,2 1例高血压非肥胖患者 ,2 3例高血压合并肥胖患者禁食 12h后 ,进行标准脂肪负荷试验 ,以TG 8h曲线下面积 (TG AUC)和TG峰反应 (TGPR)作为标准脂肪负荷后TG反应水平的指标。以胰岛素敏感性指数 (ISI)及胰岛素曲线下面积 (IS AUC)作为胰岛素敏感性的判定指标。结果　 (1)高血压合并肥胖、高血压非肥胖、单纯肥胖组TG AUC ,TGPR均显著高于正常组 [TG AUC分别为 :(2 4 5 1± 10 6 8)mmol/L、(17 5 8± 7 6 8)mmol/L、(15 2 6± 4 93)比 (8 74± 2 34)mmol/L ,P <0 0 5 ;TGPR分别为 :(5 2 1± 2 2 7)mmol/L、(3 4 6± 1 82 )mmol/L、(3 0 2± 1 0 1)比 (1 5 4±0 5 6 )mmol/L ,P <0 0 5 ],高血压合并肥胖组TG AUC ,TGPR显著高于高血压非肥胖和单纯肥胖组 (P<0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (2 )高血压合并肥胖、高血压非肥胖、单纯肥胖组ISI(绝对值 ) ,IS AUC均显著高于正常组 ,高血压合并肥胖组IS AUC ,ISI显著高于高血压非肥胖和单纯肥胖组 (P <0 0 1) ,高血压非肥胖组与单纯肥胖组之间无显著性差异。 (3)高血压合并肥胖、高血压非肥胖和肥胖组中具     

高血压病患者脂餐后甘油三酯代谢变化与血管内皮功能的关系

目的本研究旨在探讨高血压病(EH)患者脂餐后甘油三酯(TG)变化及其与血管内皮功能之间的关系.方法38例EH患者和20例健康人禁食10～12h后,采用高分辨率彩色血管超声、以肱动脉反应性充血前、后血管内径变化百分比反映血管内皮依赖性扩张功能.随后进行标准脂肪负荷试验,以TG8h曲线下面积(TG-AUC)和TG峰反应(TGPR)作为标准脂肪负荷后TG反应水平的指标.结果(1)EH组的肱动脉反应性充血前、后血管内径变化百分比显著小于对照组[(10.36±3.43)%比(15.48±4.36)%P<0.05];(2)EH组餐后TG水平的TGPR[(4.68±1.74)mmol/L比(1.84±0.67)mmol/L]及TG-AUC[(23.59±6.48)mmol/L比(9.49±3.47)mmol/L]均显著大于对照组(P<O.05);(3)EH合并餐后TG代谢障碍组(n=26)的肱动脉反应性充血前、后血管内径变化百分比较EH餐后TG代谢正常组(n=12)有明显降低[(10.98±1.32)%比(13.14±1.09)%,P<0.05].结论68.4%的EH患者伴有脂餐后TG代谢障碍和消除延迟,餐后TG代谢异常会加重EH患者血管内皮功能障碍.     

血脂康改善冠心病患者餐后高甘油三酯血症

目的 :观察冠心病患者高脂餐后血脂的变化以及 6周血脂康对餐后血脂水平的影响。　　方法 :5 0例病情稳定的冠心病患者随机分为两组 ,分别在常规治疗的基础上服用血脂康 (每日 12 0 0mg ,血脂康组 ,n =2 5 )和安慰剂 (常规组 ,n =2 5 )。所有患者在治疗前和治疗后各接受 1次高脂餐 (总热量 80 0千卡 ,脂肪 5 0克 ) ,采集空腹 12h、餐后 2、 4、 6h静脉血备测血清甘油三酯、总胆固醇、低密度脂蛋白胆固醇 (LDL C)和高密度脂蛋白胆固醇(HDL C)浓度。　　结果 :5 0例患者治疗前餐后 2、 4、 6h与空腹状态比较 ,血清甘油三酯浓度显著升高 (P <0 0 5 )。血脂康组治疗后较治疗前空腹血清甘油三酯、总胆固醇、LDL C浓度显著降低 ,HDL C浓度显著升高 ,均有极显著差异 (P均 <0 0 0 1) ;血脂康组治疗后较治疗前的餐后 2、 4和 6h血清甘油三酯浓度和甘油三酯曲线下面积明显下降 (P <0 0 5 )。常规组的空腹和餐后血脂水平较治疗前无显著变化。　　结论 :血脂康能有效降低冠心病患者空腹血脂浓度和高脂餐后升高的血清甘油三酯浓度。     

老年糖尿病患者脂肪餐后甘油三酯的变化及其对血管内皮功能的影响

目的探讨老年糖尿病患者餐后甘油三酯(TG)的动态变化及其对血管内皮功能的影响。方法随机选取空腹血脂正常的老年2型糖尿病患者及非糖尿病患者各30例,进行6 h口服脂肪餐试验,应用高分辨超声检测空腹及餐后4 h的颈动脉内-中膜厚度(IMTc)与肱动脉血流介导的血管舒张功能(FMD)。结果两组脂肪餐后TG水平均较空腹时显著增高,但糖尿病组TG曲线下面积(TG-AUC)显著高于非糖尿病组[(10．46±2,34)mmol／L对(6．48±1．26)mmol／L,P< 0．05];两组餐后IMTc均无明显改变,但FMD明显受损,糖尿病组餐后FMD下降程度(△FMD)明显高于非糖尿病组[(53．02±25．50)％对(29．19±20．42)％,P<0．05]。相关分析显示,糖尿病组TG-AUC与餐后4 h TG增加值(△TG4)呈正相关(r=0．79,P<0．05);其△FMD与△TG2呈独立相关(r=0．74,P<0．05)。结论老年糖尿病患者存在餐后高TG血症,它可导致血管内皮功能受损,促进动脉粥样硬化的发生与发展。     

高脂餐与空腹顿服胺碘酮的药代动力学对比研究

目的　比较空腹和高脂餐后顿服胺碘酮的药代动力学变化 ,探讨饮食对胺碘酮药代动力学的影响。方法　 8名健康男性志愿者 ,年龄 (2 1 6± 1 2 )岁 ,体重 (6 5 8± 5 6 )kg。志愿者分别在空腹12h和进食标准脂肪早餐 (含黄油 1 5 g/kg体重 )后顿服胺碘酮 80 0mg ,两次服药间隔 12周。高效液相色谱法测定胺碘酮及其代谢产物去乙基胺碘酮浓度 ,计算餐后与空腹服药后药代动力学参数及相对生物利用度。结果　结果显示高脂餐后胺碘酮的血浆浓度较空腹服药明显增高。餐后胺碘酮的峰浓度(Cmax)和血药浓度 时间曲线下面积 (AUC0 t)均较空腹服药显著升高 [Cmax(2 330± 12 14)ng/ml对 (90 3± 35 3)ng/ml;AUC0 t(2 72 6 6± 86 6 7)ng·h·ml-1对 (12 82 5± 5 985 )ng·h·ml-1](P <0 0 1) ;消除半衰期 (t1/ 2 )明显延长 [(2 9 6± 9 8)h对 (17 0± 5 3)h](P <0 0 1) ;达到峰值时间 (Tmax)基本不变 [(4 6±1 2 )h对 (4 6± 1 5 )h]。根据各受试者的AUC计算出高脂餐后服药的相对生物利用度为 2 39%±75 %。结论　高脂餐后服药增加胺碘酮的吸收 ,显著增加胺碘酮的血药浓度 ,同时减慢胺碘酮自体内的消除 ,提示进食高脂餐可能影响药物的疗效。     

老年人冠心病确诊前血脂变化研究

目的　研究老年人冠心病确诊前血脂变化特点。方法　确诊冠心病当年及前 4年的总胆固醇 (TC)、甘油三酯 (TG)、低密度脂蛋白胆固醇 (L DL )和高密度脂蛋白胆固醇 (HDL)水平并进行比较。结果　冠心病组与无冠心病组血脂比较 :TC5.1 5± 0 .91 mmol/ L与 5.0 2± 0 .98mmol/L,TG1 .55± 0 .86mmol/ L与 1 .53± 0 .96mmol/ L,HDL 1 .33± 0 .34mmol/ L与 1 .46± 0 .45mmol/ L,LDL3.1 2± 0 .94mmol/ L与 2 .73± 0 .79mmol/L ,LDL/ HDL2 .53± 1 .0 9与 1 .91± 0 .66。研究组确诊当年、前 1年、前 2年、前 3年和前 4年的血脂变化 :HDL1 .33± 0 .34、1 .30± 0 .37、1 .34± 0 .31、1 .32± 0 .35和 1 .43± 0 .44;LDL3.1 2± 0 .94、3.2 3± 0 .98、3.0 4± 0 .86、2 .33± 0 .99和 2 .89± 0 .96。结论　冠心病危险因子在确诊冠心病前的第1年最高 ,提示在进入老年期血脂仍旧在改变 ,冠心病危险因子不断升高 ,保护因子不断降低 ;老年人仍有必要采取干预血脂措施。     

2型糖尿病大血管病变相关因素多元回归分析——餐后甘油三酯水平增高可能为独立危险因素

目的　探讨影响 2型糖尿病大血管病变的危险因素。方法　初诊 2型糖尿病 2 6 8例按是否合并大血管病变分为病变组 (98例 )及对照组 (170例 ) ,对其进行混合餐负荷试验及其相关的临床观察 ,筛选相关因素进行多元逐步L ogistic回归分析。结果　病变组体重指数 (BMI) 2 5 .6 6± 1.78kg/ m2 较对照组 2 3.0 4± 1.6 8kg/ m2 增高 (P <0 .0 5 ) ;病变组餐后 4小时 TG水平 3.2 3± 0 .89mmol/ L 较对照组 1.99± 0 .79mmol/ L 增高 (P <0 .0 5 ) ;将 2 6 8例受试者作为整体 ,以大血管病变作为应变量 Y(有 =1;无 =0 ) ,以年龄、BMI、收缩压 (SBP)、舒张压 (DBP)、糖化血红蛋白 (Hb A1c)、空腹胰岛素 (FINS)、空腹 TG、TC、L DL- C、HDL- C及餐后 4小时甘油三酯 (TG4 h)共 11个因素为自变量 ,进行多元逐步L ogistic回归分析 ,入选的变量是 TG4 h和 BMI。结论　提示餐后甘油三酯水平增高与糖尿病大血管病变独立显著相关 ,应重视糖尿病患者的调脂治疗     

阻塞型睡眠呼吸暂停综合征与胰岛素抵抗的关系

目的　探讨阻塞型睡眠呼吸暂停综合征 (OSAS)低氧与胰岛素抵抗之间的关系及持续正压通气 (CPAP)治疗OSAS对胰岛素抵抗的影响。方法　分析 6 1例OSAS患者CPAP治疗前后及 16例未治疗OSAS患者多导睡眠监测各项指标与空腹血糖、胰岛素和餐后 2h血糖、胰岛素的关系 ,另选择 5 6例不符合SAS诊断者为对照组。结果　OSAS组治疗前呼吸紊乱指数 ( 36 .4±18.2 )次 /h ,最低氧饱和度 ( 74.5± 6 .2 ) % ,餐后血糖 ( 10 .6± 2 .4)mmol/L ,餐后胰岛素 ( 6 9.7±2 7.7)uIU/ml,胰岛素敏感性 ( 0 .8± 0 .2 )。CPAP治疗第 10天复查上述各项指标结果分别为 ( 3.3± 3.4)次 /h、( 86 .5± 1.3) %、( 7.2± 0 .6 )mmol/L、( 39.7± 10 .2 ) μIU/ml、1.2± 0 .2。P值分别 <0 .0 1、<0 .0 1、<0 .0 5、<0 .0 1、<0 .0 1。结论　OSAS组治疗前血浆胰岛素和血糖比对照组高 ,治疗后OSAS组比未治疗组低。表明OSAS低氧可产生胰岛素抵抗。     

脂餐负荷后血清甘油三酯反应水平与颈动脉内中膜厚度的关系

探讨餐后血浆富含甘油三酯脂蛋白蓄积与劝脉粥样硬化的关系。方法４２例经冠状动脉造影证实的男性冠心病患者接受了标准口服脂肪餐负荷试验,分别于餐前及虎后２、４、６、８小时测定血清甘油三酯浓度及空腹血清载脂蛋白Ｂ、高密度脂蛋白胆固浓度。     

代谢综合征患者餐后三酰甘油水平

目的探讨代谢综合征（MS）患者口服脂肪餐试验后三酰甘油（TG）浓度的变化。方法住院MS患者42例年龄（56．4&#177;10．2）岁作为实验组，另有正常者21例年龄（58．9&#177;10．0）岁作为对照组。两组均口服脂肪餐（脂肪含量62％，53．4g／m^2体表面积）并分别测定空腹，餐后2h、4h、6h、8h、10h的TG浓度，用餐后TG浓度的曲线下面积（AUC）反映餐后TG的反应及代谢能力。结果空腹胰岛素水平、胰岛素抵抗指数及体质量指数（BMI）实验组均显著高于对照组（P〈0．05，P〈0．01，P〈0．01）。实验组患者餐后TG的AUC值与高峰浓度均显著高于对照组[实验组：（22．4&#177;14．2）比对照组：（10．3&#177;6．1）mmol／（L&#183;h），实验组：（6．0&#177;2．0）比对照组：（3．1&#177;1．3）mmol／（L&#183;h），P均〈O．01]。餐后TG平均高峰浓度实验组出现在餐后6h，与对照组出现在餐后4h相比明显后延。多元线性回归分析以空腹TG、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）水平、年龄、BMI及胰岛素抵抗指数作为自变量。发现只有空腹TG水平是AUC水平的独立预测因子（B=10．3，P〈0．01）。结论MS患者餐后TG的反应水平比正常人显著升高，且清除延缓；餐后TG代谢失衡应是MS的重要特征之一。空腹TG水平是MS患者餐后TG代谢失衡的最主要的影响。     

Effects of Simvastatin on Fasting and Postprandial Triglyceride-Rich Lipoproteins in Patients with Type I Diabetes Mellitus

To assess the effect of simvastatin on fasting and postprandial triglyceride (TG)-rich lipoproteins in subjects with type 1 diabetes and elevated LDL cholesterol levels, eight patients participated in a simvastatin versus placebo, randomized, crossover study. At the end of each drug period fasting and postprandial lipoprotein studies were undertaken. Fasting plasma total and LDL cholesterol and apolipoprotein B (apo B) were significantly lower on simvastatin compared to placebo. Postprandial studies: simvastatin versus placebo consistently decreased the area under the curve (AUC, mean ± SEM) of TG in plasma (12.52 ± 9.07 versus 18.70 ± 10.48 mmol × h/L, p = 0.02). Similarly, TG AUC was lower: in the chylomicron subfraction (S_f > 400) 3.24 ± 2.71 versus 5.27 ± 4.61 mmol × h/L p = 0.03; and in the [chylomicron remnant + VLDL] subfraction (S_f 20–400) 3.98 ± 2.51 versus 7.04 ± 3.88 mmol × h/L, p = 0.01. This was due to decreased particle number rather than size, as shown by a decrease in the AUC of apo B in S_f 20–400 (600 ± 360 versus 980 ± 600 mg × h/L, p = 0.02) and the lack of change in the ratio of TG/apo B. Intestinal lipoproteins contributed to the simvastatin effect, as shown by the lower AUC of retinyl esters in both subfractions. Chylomicrons: 627.61 ± 363.43 versus 948.19 ± 568.34 nmol × h/L, p = 0.02 and remnants: 129.23 ± 67.12 versus 208.49 ± 92.11 nmol × h/L, p = 0.04. Our data suggest an additional mechanism by which simvastatin can decrease the risk of atherosclerosis in patients with type I diabetes: a decrease of the number of circulating intestinal and hepatic postprandial TG-rich lipoprotein particles.     

Exacerbation of insulin resistance and postprandial triglyceride response in newly diagnosed hypertensive patients with hypertriglyceridaemia

The purpose of the study is to examine the differences in insulin resistance and postprandial triglyceride (TG) response between hypertensive patients with or without hypertriglyceridaemia. The study is a comparative cohort study with matching. Thirty-one newly diagnosed hypertensive patients without any medication were recruited from a health survey. The participants were further divided into two groups: those with fasting TG <2.26 mmol/L, and those with TG between 2.26 and 5.65 mmol/L. Both groups were matched in age, sex, body mass index and waist circumference. Each patient received a 75-g oral glucose tolerance test, an insulin suppression test, and a 1000 kcal high fat mixed meal test. The hypertriglyceridaemic hypertensive patients had significantly higher fasting insulin, 2-h plasma glucose, 2-h insulin, and steady-state plasma glucose (SSPG) (13.16 +/- 1.87 vs 9.76 +/- 3.18 mmol/L). They also had a greater postprandial TG response to the challenge of mixed meal (DeltaAUC 20.76 +/- 10.06 vs 7.97 +/- 3.18 mmol 8 h/L). The postprandial TG response was closely correlated (r = 0.72-0.95, P < 0.0001) with fasting TG in all hypertensive patients. Both fasting TG levels and postprandial TG response were significantly (P < 0.05) correlated with SSPG. In conclusion, the hypertensive patients with hypertriglyceridaemia were more insulin resistant than those without it. Exacerbation of postprandial hypertriglyceridaemia was identified in these patients. The TG response to the challenge of high fat meal was significantly correlated with fasting TG and insulin resistant in them. The results provide a rationale for the alleviation of insulin resistance and hypertriglyceridaemia in these atherosclerosis-prone hypertensive patients.     

单纯性肥胖青少年血清脂蛋白亚组分水平分析

目的探讨青少年单纯性肥胖与血清脂蛋白及其亚组分水平的关系。方法采用超速离心-高效液相色谱法测定60例肥胖青少年和19例体重指数正常者血清脂蛋白及其亚型水平。使用双能量X线吸收仪检测所有受试者全身及躯干部体脂比率。结果与正常对照组相比,肥胖组血清TC(4.47±0.90)比(3.79±0.50)mmol/L、TG(1.02±0.41)比(0.72±0.34)mmol/L、LDL-C(2.56±0.81)比(1.95±0.35)mmol/L、LDLa-C(2.39±0.83)比(1.74±0.37)mmol/L平均水平显著增高,而HDL-C(1.18±0.23)比(1.35±0.16)mmol/L、HDL2-C(0.73±0.21)比(0.91±0.16)mmol/L平均水平明显降低(P<0.01)。BMI、腰围、全身体脂及躯干体脂比率分别与TC、TG、LDL-C、LDLa-C水平呈显著正相关,与HDL-C、HDL2-C水平呈显著负相关(P<0.05,P<0.01)。结论单纯性肥胖青少年存在与肥胖相关的早期脂质代谢紊乱的趋势。     

Hepatic fat content is a determinant of postprandial triglyceride levels in type 2 diabetes mellitus patients with normal fasting triglyceride

Postprandial hypertriglyceridemia is common in type 2 diabetes mellitus (T2D). Significant numbers of T2D patients who have normal fasting triglyceride (TG) have postprandial hypertriglyceridemia. The role of regional adipose tissue and adiponectin on postprandial TG responses in this group of T2D patients is unclear. This study aimed to examine the contribution of regional adipose tissue and adiponectin to the variation of postprandial TG responses in T2D patients who have normal fasting TG levels. Thirty-one Thai T2D patients who had fasting TG<1.7 mmol/L were studied. All were treated with diet control or sulphonylurea and/or metformin. None was treated with lipid-lowering agents. Mixed-meal test was performed after overnight fast. Plasma glucose, insulin, and TG were measured before and 1, 2, 3, and 4 hours after the test. Adiponectin was measured in fasting state. Visceral as well as superficial and deep subcutaneous abdominal adipose tissues were determined by magnetic resonance imaging, and hepatic fat content (HFC) was determined by magnetic resonance spectroscopy. Univariate and multivariate regression analyses of postprandial TG and regional adipose tissue and metabolic parameters were performed. The TG levels before and 1, 2, 3, and 4 hours after the mixed meal were 1.32+/-0.40 (SD), 1.40+/-0.41, 1.59+/-0.40, 1.77+/-0.57, and 1.80+/-0.66 mmol/L, respectively (P<.0001). The area under the curve (AUC) of postprandial TG was positively and significantly correlated with fasting TG (r=0.84, P<.0001) and log.HFC (r=0.456, P=.033) and was inclined to be correlated with log.deep subcutaneous adipose tissue (r=0.38, P=.05) and sex (r=0.326, P=.073). The AUC of postprandial TG was not correlated with age, body mass index, waist circumference, log.superficial subcutaneous adipose tissue, log.visceral adipose tissue, hemoglobin A1c, fasting glucose, AUC.glucose, log.fasting insulin, log.AUC.insulin, log.homeostasis model assessment%B, log.homeostasis model assessment of insulin resistance, and adiponectin. Only fasting TG (beta=.815, P<.0001) and log.HFC (beta=.249, P=.035) predicted AUC of postprandial TG in regression model (adjusted R2=0.84, P<.0001). In conclusion, in T2D patients with normal fasting TG, the increase of postprandial TG levels is directly determined by fasting TG level and the amount of hepatic fat.     

Effect of xuezhikang,a cholestin extract,on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease

The effect of xuezhikang on postprandial triglyceride (TG) level was investigated in patients with coronary heart disease (CHD) after a high-fat meal (800 cal; 50 g fat). Fifty CHD patients were randomly divided into two groups to accept xuezhikang (xuezhikang group) 1200 mg/day (600 mg twice daily) or not (control group) on the base of routine therapy which included aspirin, metoprolol and fosinopril and nitrates during the whole 6 weeks following-up. Xuezhikang significantly reduced fasting serum total cholesterol (TC) (-20%), low-density lipoprotein cholesterol (LDL-C, -34%), TG (-32%) and apoB (-27%) levels, and raised fasting high-density lipoprotein cholesterol (HDL-C, 18%) and apoA-I (13%) levels (P<0.001). The postprandial serum TG levels at 2, 4 and 6 h decreased 32, 38 and 43%, respectively, in xuezhikang group (P<0.001). The TG area under the curve over the fasting TG level (TG-AUC) significantly decreased in CHD patients accepted xuezhikang with normal (less than 1.7 mmol/l) and elevated (1.74 to 2.92 mmol/l) fasting TG levels by 45 and 50%, respectively (P<0.001). Routine therapy had no significant effect on the fasting and postprandial lipid and apolipoprotein levels. The change of TG-AUC was significantly related to the changes of fasting TG, TC, LDL-C, and HDL-C levels after the treatment, which were related to the changes of fasting apoA-I and apoB levels significantly (P<0.001). Xuezhikang was shown to be beneficial in the treatment of reflecting postprandial triglyceridemia in CHD patients with normal and mildly elevated fasting TG levels.     

Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size

The fasting atherogenic dyslipidemia of visceral obesity, which includes the presence of small, dense low-density lipoprotein (LDL) particles, is predictive of an increased risk of coronary heart disease (CHD). It has also been suggested that progression of atherosclerosis may be accelerated in the presence of postprandial hyperlipidemia independently from the fasting dyslipidemic state. Studies have shown that the best predictor of postprandial hyperlipidemia and of the small, dense LDL phenotype is fasting triglyceride (TG) concentration. In the present study, we evaluated the impact of postprandial hypertriglyceridemia on the variation in LDL particle size. Fasting (0 hour) and postprandial changes (2, 4, 6, and 8 hours) in LDL particle size were measured by nondenaturing 2% to 16% polyacrylamide gel electrophoresis in a sample of 49 men (mean age +/- SD: 46.6 +/- 9.2 years) who underwent a standardized breakfast with a high-fat (64% calories as fat) content. The postprandial increase in TG levels was associated with a transient reduction in LDL particle size, the most substantial reduction being observed 4 hours (-1.0 +/- 2.4 A) after the oral fat load. Although there were strong correlations between TG-rich lipoprotein (TRL)-TG levels and LDL particle size in the fasting state (r=-0.71, P<.0001) as well as 4 hours after the oral fat load (r=-0.70, P<.0001), changes in TRL-TG concentrations during the postprandial state (from time 0 to 4 hours) were not associated with changes in LDL particle size during this period (r=-0.04, not significant [NS]). However, among subgroups of men matched for similar fasting TRL-TG levels (n=12), subjects with the highest total area under the curve (AUC) of TRL-TG after the fat load were characterized by smaller LDL particle size at 6 and 8 hours compared with men with the lowest AUC TRL-TG (P<.02). Men displaying the highest postprandial AUC TRL-TG were also characterized by the greatest accumulation of visceral adipose tissue (AT) (P<.05). These results indicate that the hypertriglyceridemic (hyperTG) state induced by a high-fat meal is associated with a transient reduction in LDL peak particle diameter, which is not proportionate, however, to the level of TG achieved in the postprandial state. Furthermore, despite similar TG levels at baseline, viscerally obese men with an impaired postprandial lipemia had smaller LDL particles at the end of the oral fat load than obese men with a lower accumulation of visceral AT.     

Postprandial hyperlipidemia: another correlate of the "hypertriglyceridemic waist" phenotype in men

Fasting hypertriglyceridemia has been reported to be predictive of an exaggerated triglyceride (TG) response to an oral fat load. Abdominal obesity has also been associated with postprandial hyperlipidemia. The objective of the present study was to quantify the contribution of abdominal obesity and fasting hypertriglyceridemia to the magnitude of postprandial lipemia. For that purpose, potential differences in postprandial TG-rich lipoprotein (TRL) levels were examined among men characterized by the absence/presence of the "hypertriglyceridemic waist" phenotype following a standardized breakfast with a high fat content (64% calories as fat). Sixty-nine men (mean age +/- S.D.: 45.1 +/- 10.5 years) were classified according to waist girth (< 90 or >/ or = 90 cm) and fasting TG concentrations (< 2.0 or > or = 2.0 mmol/l). Subjects characterized by "hypertriglyceridemic waist" (waist > or = 90 cm and fasting TG > or = 2.0 mmol/l) showed the highest TRL-TG concentrations (P < 0.0001) throughout the entire postprandial period (8 h) as well as elevated concentrations of apolipoprotein (apo) B-48 and apo B-100 in all TRL fractions (large, medium and small) compared to subjects with low fasting TG levels who had waist girth values either above or below 90 cm. These higher postprandial TRL-TG levels among carriers of the "hypertriglyceridemic waist" phenotype also led to significantly greater postprandial TG-total area under the curve (AUC) in total TRLs resulting mainly from the increased concentrations of large- and medium-sized TRLs. Furthermore, subjects characterized by the "hypertriglyceridemic waist" phenotype displayed higher fasting insulin concentrations and postprandial insulin AUC compared to men with low fasting plasma TG levels and low waist girth values. In conclusion, results of the present study indicate that postprandial hyperlipidemia is associated with the simultaneous presence of abdominal obesity and elevated fasting TG concentrations: a condition that we have described as the "hypertriglyceridemic waist" phenotype.