Cohen Rairaja, Sheftel Jesse, Luevano Jennifer, Kelly Meredith O, Fanter Rob K, van Stuijvenberg Martha E, Dhansay Muhammad A, Brito Alex, Tanumihardjo Sherry A, La Frano Michael R
Department of Food Science and Nutrition, California Polytechnic State University, San Luis Obispo, CA, USA.
University of Wisconsin-Madison, Madison, WI, USA.
Br J Nutr. 2025 Jun 14;133(11):1385-1394. doi: 10.1017/S0007114525103656. Epub 2025 Jun 17.
Evidence indicates hypervitaminosis A may be attributed to overconsumption of natural preformed vitamin A (VA) and overlapping VA intervention strategies. Hypervitaminosis A can disrupt metabolic processes; however, the extent and mechanisms of these impacts are not well understood. This study aims to assess metabolic differences related to hypervitaminosis A and VA supplementation by performing metabolomics analysis. A subsample of South African preschoolers participating in the country's VA supplementation programme was selected. Participants were divided into two groups: adequate VA ( 15; 0·59-0·99 µmol/g total liver reserve and high VA ( 15; ≥ 1·0 µmol/g total liver reserve). Serum samples were collected at baseline and 28 d after consuming a 200 000 IU VA supplement. Lipidomics and oxylipins assays were conducted using ultraperformance LC-MS. At baseline, unsaturated lysophosphatidylcholines and unsaturated phosphatidylcholines were significantly lower in the high VA group ( < 0·05). A group-by-time interaction with VA supplementation was observed for polyunsaturated lysophosphatidylcholines and polyunsaturated phosphatidylcholines ( < 0·05). Additionally, a group effect was noted for oxylipins, and a time effect in response to VA supplementation was seen with decreased arachidonic acid and lipoxygenase- and non-enzymatically derived oxylipins ( < 0·05). Hypervitaminosis A is associated with modifications in lipids involved in cell structure and signalling, particularly unsaturated lysophosphatidylcholines and phosphatidylcholines. Further research is needed to identify the mechanisms behind these modifications, their physiological effects and their potential as biomarkers of elevated vitamin A status.
有证据表明，维生素A过多症可能归因于天然预形成维生素A（VA）的过量摄入以及VA干预策略的重叠。维生素A过多症会扰乱代谢过程；然而，这些影响的程度和机制尚未完全了解。本研究旨在通过进行代谢组学分析来评估与维生素A过多症和VA补充相关的代谢差异。选取了参与该国VA补充计划的南非学龄前儿童的一个子样本。参与者被分为两组：VA充足组（15；总肝储备量为0·59 - 0·99 µmol/g）和高VA组（15；总肝储备量≥1·0 µmol/g）。在基线时以及服用200 000 IU VA补充剂28天后采集血清样本。使用超高效液相色谱 - 质谱联用仪进行脂质组学和氧化脂质测定。在基线时，高VA组中不饱和溶血磷脂酰胆碱和不饱和磷脂酰胆碱显著较低（<0·05）。对于多不饱和溶血磷脂酰胆碱和多不饱和磷脂酰胆碱，观察到与VA补充存在组 - 时间交互作用（<0·05）。此外，氧化脂质存在组效应，并且在VA补充后观察到时间效应，表现为花生四烯酸以及脂氧合酶和非酶促衍生的氧化脂质减少（<0·05）。维生素A过多症与参与细胞结构和信号传导的脂质修饰有关，特别是不饱和溶血磷脂酰胆碱和磷脂酰胆碱。需要进一步研究以确定这些修饰背后的机制、它们的生理效应以及它们作为维生素A水平升高生物标志物的潜力。
