van Oostrom Antonie J, van Dijk Hans, Verseyden Caroline, Sniderman Allan D, Cianflone Katherine, Rabelink Ton J, Castro Cabezas Manuel
Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, Netherlands.
Am J Clin Nutr. 2004 Mar;79(3):510-5. doi: 10.1093/ajcn/79.3.510.
Elevated fasting plasma concentrations of complement component 3 (C3) are associated with elevated fasting and postprandial triacylglycerol concentrations, insulin resistance, obesity, and coronary artery disease. C3 is the central component of the complement system and the precursor of acylation-stimulating protein (ASP). Insulin and ASP are principal determinants of free fatty acid (FFA) trapping by adipose tissue.
Because controversy exists concerning postprandial changes in C3 and because meal composition may influence complement activation, we studied postprandial lipemia in relation to changes in plasma C3.
After an overnight fast, 6 healthy men ( +/- SD age: 23 +/- 2 y) underwent 4 oral liquid challenges: fat (50 g/m(2) body surface), glucose (37.5 g/m(2)), fat and glucose (mixed test), and water (as a control test) in a random, crossover design.
Plasma ASP concentrations did not change postprandially in any test. Changes in C3 concentration were observed only after the fat challenge: elevated concentrations occurred between 1 and 3 h, and a maximum increase of 11% occurred at 2 h (P = 0.05). Postprandial triacylglycerolemia did not differ significantly between the fat and mixed tests. The FFA response after the fat challenge was the highest of all the tests (P < 0.05 for all comparisons) and was accompanied by an increase in ketone bodies (maximum at 6 h); this increase did not occur after the mixed test, which suggests less hepatic FFA delivery.
When glucose is added to an oral fat load, the postprandial FFA response is reduced, and the fat-specific increase in C3 is prevented. After ingestion of fat without glucose, the lack of insulin response may lead to C3-mediated peripheral FFA trapping, which probably serves as a backup system in case of insufficient or inefficient insulin-dependent FFA trapping.
空腹血浆补体成分3（C3）浓度升高与空腹及餐后三酰甘油浓度升高、胰岛素抵抗、肥胖和冠状动脉疾病相关。C3是补体系统的核心成分及酰化刺激蛋白（ASP）的前体。胰岛素和ASP是脂肪组织捕获游离脂肪酸（FFA）的主要决定因素。
由于关于餐后C3变化存在争议，且膳食组成可能影响补体激活，我们研究了餐后血脂与血浆C3变化的关系。
6名健康男性（年龄±标准差：23±2岁）隔夜禁食后，采用随机交叉设计接受4种口服液体激发试验：脂肪（50 g/m²体表面积）、葡萄糖（37.5 g/m²）、脂肪和葡萄糖（混合试验）以及水（作为对照试验）。
在任何试验中，血浆ASP浓度餐后均未改变。仅在脂肪激发试验后观察到C3浓度变化：1至3小时浓度升高，2小时最大升高11%（P = 0.05）。脂肪试验和混合试验餐后三酰甘油血症无显著差异。脂肪激发试验后FFA反应在所有试验中最高（所有比较P < 0.05），并伴有酮体增加（6小时时最高）；混合试验后未出现这种增加，这表明肝脏FFA输送减少。
当葡萄糖添加到口服脂肪负荷中时，餐后FFA反应降低，且脂肪特异性的C3增加被阻止。在摄入不含葡萄糖的脂肪后，胰岛素反应缺乏可能导致C3介导的外周FFA捕获，这可能在胰岛素依赖性FFA捕获不足或低效时作为备用系统。
