Department of Nutrition, University of California Davis, Davis, CA, USA.
Am J Clin Nutr. 2012 Apr;95(4):851-8. doi: 10.3945/ajcn.111.028340. Epub 2012 Feb 29.
Accumulating data show a causal role for flavanols in the mediation of cardiovascular benefits associated with the consumption of flavanol- and procyanidin-containing foods. Evidence for a direct causal role for procyanidins in this context is far less profound due to the poor absorption of procyanidins. However, it has been proposed that procyanidins may break down in the gastrointestinal tract, resulting in monomeric flavanols, which contribute to the systemic flavanol pool. Verification or rejection of this supposition could significantly affect the interpretation of epidemiologic and dietary intervention data and the design of food-content databases.
We assessed the respective contribution of flavanols and procyanidins to the systemic pool of flavanols and 5-(3,4-dihydroxyphenyl)-γ-valerolactone (γ-VL) in humans.
Test drinks that contained only flavanols (D1), procyanidins with a degree of polymerization that ranged from 2 to 10 (D2-10), or flavanols and procyanidins with a degree of polymerization that ranged from 2 to 10 (D1-10) were consumed by subjects (n = 12) according to a randomized, double-masked, crossover design. Plasma and urine samples were collected postprandially and analyzed.
The ingestion of D1-10 resulted in the systemic presence of flavanols (plasma concentration: 863 ± 77 nmol/L), γ-VLs (24-h urine: 93 ± 18 μmol), and minute concentrations of procyanidin B2. With correction for small residual amounts of flavanols present in D2-10, only negligible concentrations of circulating flavanols were detected after ingestion of the drink, whereas the intake of D1 resulted in circulating flavanol concentrations similar to those detected after D1-10 consumption.
These outcomes show that dietary procyanidins do not contribute to the systemic pool of flavanols in humans. Thus, these data reject the notion that procyanidins, through their breakdown into flavanols and subsequent absorption, causally modulate vascular function.
越来越多的数据表明,黄烷醇在介导与食用富含黄烷醇和原花青素的食物相关的心血管益处方面起着因果作用。由于原花青素吸收不良,证明原花青素在这种情况下具有直接因果作用的证据要少得多。然而,有人提出原花青素可能在胃肠道中分解,产生单体黄烷醇,从而为系统性黄烷醇池做出贡献。验证或否定这种假设可能会显著影响对流行病学和饮食干预数据的解释以及食品成分数据库的设计。
我们评估了黄烷醇和原花青素对人体系统性黄烷醇池和 5-(3,4-二羟基苯基)-γ-缬草酸(γ-VL)的各自贡献。
根据随机、双盲、交叉设计,让 12 名受试者分别饮用仅含黄烷醇(D1)、聚合度为 2 至 10 的原花青素(D2-10)或黄烷醇和聚合度为 2 至 10 的原花青素(D1-10)的测试饮料。餐后收集血浆和尿液样本并进行分析。
D1-10 的摄入导致黄烷醇(血浆浓度:863±77nmol/L)、γ-VL(24 小时尿液:93±18μmol)和微量原花青素 B2 在体内存在。在对 D2-10 中存在的少量残留黄烷醇进行校正后,仅在饮用该饮料后检测到循环黄烷醇的可忽略浓度,而 D1 的摄入导致循环黄烷醇浓度与 D1-10 消耗后检测到的浓度相似。
这些结果表明,膳食中原花青素不会导致人体系统性黄烷醇池的增加。因此,这些数据否定了原花青素通过分解为黄烷醇和随后的吸收来调节血管功能的观点。