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首页> 外文期刊>British Journal of Pharmacology >Induction of cytochrome P450 1A by cow milk-based formula: a comparative study between human milk and formula.
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Induction of cytochrome P450 1A by cow milk-based formula: a comparative study between human milk and formula.

机译：基于牛奶的配方奶对细胞色素P450 1A的诱导：人奶与配方奶之间的比较研究。

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During the treatment of neonatal apnea, formula-fed infants, compared to breastfed infants, show nearly three-fold increase in clearance of caffeine, a substrate of cytochrome P450 1A (CYP1A) and in part CYP3A4. However, human milk is known to contain higher concentrations of environmental pollutants than infant formula, which are potent CYP1A inducers. To gain insight into the mechanism underlying this apparent contradiction, we characterized CYP1A and CYP3A4 induction by human milk and cow milk-based infant formula. The mRNA and protein expression of CYP1A1/1A2 were significantly induced by cow milk-based formula, but not by human milk, in HepG2 cells. Luciferase reporter assay demonstrated that cow milk-based formula but not human milk activated aryl hydrocarbon receptor (AhR) significantly. The cotreatment of 3,4-dimethoxyflavone, an AhR antagonist, abolished the formula-induced CYP1A expression. In addition, AhR activation by dibenzo[a,h]anthracene, a potent AhR agonist, was significantly suppressed by infant formula and even more by human milk. In contrast, CYP3A4 mRNA expression was only mildly induced by formula and human milk. Consistently, neither formula nor human milk substantially activated pregnane X receptor (PXR). Effects of whey and soy protein-based formulas on the AhR-CYP1A and the PXR-CYP3A4 pathways were similar to those of cow milk-based formula. In conclusion, infant formula, but not human milk, enhances in vitro CYP1A expression via an AhR-mediated pathway, providing a potential mechanistic basis for the increased caffeine elimination in formula-fed infants.
机译：在治疗新生儿呼吸暂停期间，与母乳喂养的婴儿相比，配方喂养的婴儿的咖啡因，细胞色素P450 1A（CYP1A）和部分CYP3A4的底物清除率提高了近三倍。然而，已知母乳比婴儿配方奶粉含有更高的环境污染物浓度，婴儿配方奶粉是有效的CYP1A诱导剂。为了深入了解这一明显矛盾的潜在机制，我们对人乳和基于牛乳的婴儿配方奶粉诱导CYP1A和CYP3A4进行了表征。 CYP1A1 / 1A2的mRNA和蛋白表达在HepG2细胞中被基于牛奶的配方显着诱导，而不受人乳诱导。萤光素酶报告基因测定表明，以牛奶为基础的配方奶粉不会显着激活人乳的芳基烃受体（AhR）。 AhR拮抗剂3,4-二甲氧基黄酮的共同治疗废除了该配方诱导的CYP1A表达。此外，婴儿配方奶粉显着抑制了二苯并[a，h]蒽（一种有效的AhR激动剂）对AhR的活化作用，甚至被人乳所抑制。相反，配方奶和人乳仅轻微诱导CYP3A4 mRNA表达。一致地，配方奶和人乳都没有充分激活孕烷X受体（PXR）。基于乳清和大豆蛋白的配方对AhR-CYP1A和PXR-CYP3A4途径的影响与基于牛乳的配方相似。总之，婴儿配方食品（而非人乳）通过AhR介导的途径增强体外CYP1A表达，为配方食品喂养的婴儿中咖啡因消除的增加提供了潜在的机理基础。

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