Kim Hyang Yeon, Kim Minhee, Park Hye Min, Kim Jiyoung, Kim Eun Ji, Lee Choong Hwan, Park Jung Han Yoon
Department of Bioscience and Biotechnology, Konkuk University, Seoul, Korea.
Department of Food Science and Nutrition, Hallym University, Chuncheon, Korea.
Nutrition. 2014 Nov-Dec;30(11-12):1433-41. doi: 10.1016/j.nut.2014.04.013. Epub 2014 May 9.
Our previous study revealed that chronic consumption of a high-fat diet (HFD) stimulates colon cancer progression in obesity-resistant BALB/c mice. The aim of the present study was to investigate the significant alteration of metabolites caused by tumor progression and an HFD in the serum and liver in the same mouse model.
Male BALB/c mice were fed either a control diet or a HFD for 20.5 wk. The syngeneic CT26 colon carcinoma cells were injected into the right rear flank of mice after 16 wk of feeding. Metabolites in serum and liver samples were analyzed by ultra-performance liquid chromatography-quadrupole-time-of-flight-mass spectrometry-based metabolomics.
HFD feeding and tumor injection induced changes in the choline-containing phospholipids, namely, phosphatidylcholines and lysophosphatidylcholines (lysoPCs), and lysophosphatidylethanolamines in the serum and liver. The majority of these metabolite changes were due to HFD feeding (11 in sera and 5 in livers) rather than tumors (3 in sera and 1 in livers).
The HFD- and tumor-related metabolite alterations of phospholipids, especially lysoPCs, in the liver and serum of obesity-resistant mice, suggesting that the lysoPCs are potential biomarkers for the chronic consumption of HFD in nonobese individuals.
我们之前的研究表明，长期食用高脂饮食（HFD）会促进抗肥胖的BALB/c小鼠的结肠癌进展。本研究的目的是在同一小鼠模型中，研究肿瘤进展和HFD导致的血清和肝脏中代谢物的显著变化。
雄性BALB/c小鼠分别喂食对照饮食或HFD 20.5周。喂食16周后，将同基因CT26结肠癌细胞注射到小鼠的右后腹。通过基于超高效液相色谱-四极杆-飞行时间-质谱的代谢组学分析血清和肝脏样本中的代谢物。
喂食HFD和注射肿瘤导致血清和肝脏中含胆碱的磷脂发生变化，即磷脂酰胆碱和溶血磷脂酰胆碱（lysoPCs），以及溶血磷脂酰乙醇胺。这些代谢物变化大多是由于喂食HFD（血清中11种，肝脏中5种）而非肿瘤（血清中3种，肝脏中1种）引起的。
抗肥胖小鼠肝脏和血清中与HFD和肿瘤相关的磷脂代谢物变化，尤其是lysoPCs，表明lysoPCs是非肥胖个体长期食用HFD的潜在生物标志物。
