Effect of Phytosterol Esters on Selected Serum Metabolites of Rats with Non-alcoholic Fatty Liver Disease (NAFLD)
OUYANG Pengling, GUAN Qi, QU Dan, DING Xinwen, YANG Li, SONG Lihua
2020, 41(3):
127-137.
doi:10.7506/spkx1002-6630-20181016-164
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Based on our previous studies, the effect of phytosterol esters (PSE) on selected serum small-molecule metabolites of rats with non-alcoholic fatty liver disease (NAFLD) was investigated in the present study. Further, we explored the molecular mechanism underlying the preventive effect of PSE on NAFLD. Rats were fed with a high-fat diet to establish a NAFLD animal model, and PSE fortified milk at low (0.05 g/100 g mb·d) and high (0.10 g/100 g mb·d) doses were respectively given to rats in the PSE intervention groups by intragastric administration at the same time. Serum small-molecule metabolites of NAFLD rats were detected using ultra performance liquid chromatography-quadrupole-tandem time-of-flight mass spectrometry (UPLC-Q-TOF-MS). In addition, Progenesis QI v2.3 software, UNIFI data analysis platform and Metabo Analyst were used to analyze differential serum metabolites and the metabolic pathways involving the identified differential metabolites. Our results showed that 27 metabolites were identified, including diglyceride (14:0/22:2(13Z,16Z)/0:0, 15:0/18:3 (6Z,9Z,12Z)/0:0, 16:0/20:3(8Z,11Z,14Z)/0:0, 18:1(11Z)/18:1(11Z)/0:0), glucosylceramide (d18:2/20:0), lactosylceramide (d18:1/18:1(9Z)), heneicosanedioic acid, lysophospholipid (Lyso PC) (15:0, 16:1(9Z), 20:3(5Z,8Z,11Z), 20:3(8Z,11Z,14Z), 18:1(9Z), 18:2(9Z,12Z)), phosphatidic acid(22:4(7Z,10Z,13Z,16Z)/0:0), phosphatidylcholine(16:0/20:3(5Z,8Z,11Z), 16:0/P-18:0, 18:1(11Z)/20:1(11Z), 17:1(10Z)/0:0, 20:3(8Z,11Z,14Z)/18:0, O-18:0/0:0), phosphatidylethanolamine (16:0/0:0, 18:3(6Z,9Z,12Z)/22:6(4Z,7Z,10Z,13Z,16Z,19Z), 20:3(8Z,11Z,14Z)/0:0, 18:4(6Z,9Z,12Z,15Z)/18:0), phosphatidylinositol(20:0/22:2 (13Z,16Z)) and sphingomyelin (d16:1/25:0, d18:1/24:0). The preventive effect of PSE was exerted on NAFLD probably through correcting high-fat diet-induced disturbance of the glycerophospholipid and lipid metabolism pathways.