Human Nutrition Program, The Ohio State University, Columbus, OH 43210, USA.
Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
Nutrients. 2023 Sep 17;15(18):4021. doi: 10.3390/nu15184021.
Catechins in green tea extract (GTE) (epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin (EC), epicatechin gallate (ECG)) vary in bioactivity. We developed a physiologically relevant mathematical model of catechin metabolism to test the hypothesis that fractional catabolic rates of catechins would be differentially affected by their structural attributes. Pharmacokinetic data of plasma and urine catechin concentrations were used from healthy adults ( = 19) who ingested confections containing 0.5 g GTE (290 mg EGCG, 87 mg EGC, 39 mg EC, 28 mg ECG). A 7-compartmental model of catechin metabolism comprised of the gastrointestinal tract (stomach, small and large intestine), liver, plasma, extravascular tissues, and kidneys was developed using a mean fraction dose of EGCG, ECG, EGC, and EC. Fitting was by iterative least squares regression analysis, and goodness of fit was ascertained by the estimated variability of parameters (FSD < 0.5). The interaction of gallation and B-ring dihydroxylation most greatly extended plasma residence time such that EGC > EC = EGCG > EGC. The interaction between gallation and B-ring dihydroxylation accelerated the transfer from the upper gastrointestinal tract to the small intestine but delayed subsequent transfers from the small intestine through the liver to plasma and from kidneys to urine. Gallation and B-ring dihydroxylation independently delayed the transfer from plasma to extravascular tissues, except the uptake to kidneys, which was slowed by gallation only. This multi-compartment model, to be validated in a future study, suggests that gallation and B-ring dihydroxylation affect catechin catabolism in a tissue-specific manner and thus their potential bioactivity.
绿茶提取物（GTE）中的儿茶素（表没食子儿茶素没食子酸酯（EGCG）、表儿茶素（EGC）、表儿茶素没食子酸酯（ECG））的生物活性不同。我们开发了一个与生理学相关的儿茶素代谢数学模型，以检验这样一个假设，即儿茶素的部分分解代谢率将因其结构属性的不同而受到不同的影响。使用来自健康成年人（n = 19）的血浆和尿液儿茶素浓度的药代动力学数据，这些成年人摄入了含有 0.5 g GTE（290 mg EGCG、87 mg EGC、39 mg EC、28 mg ECG）的糖果。一个由胃肠道（胃、小肠和大肠）、肝脏、血浆、血管外组织和肾脏组成的 7 室儿茶素代谢模型是使用 EGCG、ECG、EGC 和 EC 的平均分数剂量开发的。通过迭代最小二乘法回归分析进行拟合，并通过参数估计变异性（FSD < 0.5）确定拟合优度。加酯化和 B 环二羟基化的相互作用极大地延长了血浆半衰期，使得 EGC > EC = EGCG > EGC。加酯化和 B 环二羟基化的相互作用加速了从上消化道向小肠的转移，但随后从小肠通过肝脏向血浆和从肾脏向尿液的转移被延迟。加酯化和 B 环二羟基化独立地延迟了从血浆向血管外组织的转移，除了肾脏摄取，只有加酯化会减缓这一过程。这个多室模型，将在未来的研究中进行验证，表明加酯化和 B 环二羟基化以组织特异性的方式影响儿茶素的分解代谢，从而影响其潜在的生物活性。
