Charlesworth J A, Peake P W, Campbell L V, Pussell B A, O'Grady S, Tzilopoulos T
Department of Nephrology, Prince Henry Hospital, Little Bay, New South Wales, Australia.
Int J Obes Relat Metab Disord. 1998 Nov;22(11):1096-102. doi: 10.1038/sj.ijo.0800733.
To examine the hypothesis that a sustained rise in plasma acylation stimulating protein (ASP, C3a desarg) accompanies the elevation in triacylglycerol that follows the ingestion of an oral fat load.
Following an overnight fast, blood samples were obtained from healthy volunteers while fasting and 15 min, 1, 2, 4, 6 and 8 h following ingestion of: (i) a liquid meal, rich in dairy fat (eight subjects) and (ii) a semi-liquid meal, with higher total fat content and rich in polyunsaturated fat (six subjects).
Four male and four female volunteers (age range: 22-51 y; body mass index (BMI): 17.9-26.9 kg/m2) received the first meal. Six subjects (age range: 32-60 y; BMI: 18.0-28.4 kg/m2), including three from the first study, received the second meal using the same protocol. ASP and C5a were measured by radioimmunoassay (RIA) and the complement proteins C3, factor B and C5 by radial immunodiffusion or nephelometry. Tumour necrosis factor (TNF)-alpha was measured by enhanced ELISA, and plasma cholesterol and triacylglycerol by an automated enzymatic method. The presence of chylomicrons was assessed in post-prandial plasma samples taken after the second meal.
There was no significant change in mean ASP concentration in either group at any time point, following ingestion of either meal. However, there was a significant positive linear trend in ASP following the second fat challenge (ANOVA; P < 0.05). There was also no change in complement proteins, plasma cholesterol or TNF-alpha. Plasma triacylglycerol rose significantly after the first and second meals (P < 0.05 and P < 0.001 at 2 h post-prandially); the mean maximum rise above the fasting level was 58 +/- 41% and 89 +/- 38% respectively (mean +/- s.d.). Chylomicrons were detected in samples taken from each subject after the second meal. Analysis of individual ASP data showed a sustained rise in one subject after the first meal and two subjects after the second meal. Substantial variation in ASP concentration was observed in samples taken in the first 2 h post-prandially.
There was no significant change in ASP nor other complement proteins for either group of subjects following ingestion of the lipid loads. Individual data showed substantial variation in post-prandial ASP, but multiple plasma sampling did not define the basis for this variation.
检验如下假设，即摄入口服脂肪负荷后三酰甘油升高的同时，血浆酰化刺激蛋白（ASP，C3a去精氨酸）持续上升。
在健康志愿者过夜禁食后，分别在禁食时以及摄入以下食物后15分钟、1、2、4、6和8小时采集血样：（i）富含乳脂肪的流食（8名受试者），以及（ii）总脂肪含量更高且富含多不饱和脂肪的半流食（6名受试者）。
4名男性和4名女性志愿者（年龄范围：22 - 51岁；体重指数（BMI）：17.9 - 26.9kg/m²）接受第一餐。6名受试者（年龄范围：32 - 60岁；BMI：18.0 - 28.4kg/m²），包括来自第一项研究的3名受试者，按照相同方案接受第二餐。采用放射免疫分析法（RIA）测定ASP和C5a，采用放射免疫扩散法或散射比浊法测定补体蛋白C3、B因子和C5。采用增强酶联免疫吸附测定法（ELISA）测定肿瘤坏死因子（TNF）-α，采用自动酶法测定血浆胆固醇和三酰甘油。在第二餐餐后采集的血浆样本中评估乳糜微粒的存在情况。
两组受试者在摄入任何一餐之后的任何时间点，平均ASP浓度均无显著变化。然而，在第二次脂肪激发后，ASP呈现显著的正线性趋势（方差分析；P < 0.05）。补体蛋白、血浆胆固醇或TNF-α也没有变化。第一餐和第二餐之后血浆三酰甘油显著升高（餐后2小时分别为P < 0.05和P < 0.001）；高于禁食水平的平均最大升幅分别为58±41%和89±38%（平均值±标准差）。在第二餐之后采集的每个受试者样本中均检测到乳糜微粒。对个体ASP数据的分析显示，第一餐之后有1名受试者、第二餐之后有2名受试者的ASP持续升高。在餐后最初2小时采集的样本中观察到ASP浓度存在很大差异。
两组受试者在摄入脂质负荷后，ASP以及其他补体蛋白均无显著变化。个体数据显示餐后ASP存在很大差异，但多次血浆采样并未明确这种差异的原因。
