Department of Cell and Tissue Engineering, Changhua Christian Hospital, Changhua, Taiwan.
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
J Food Drug Anal. 2017 Oct;25(4):919-930. doi: 10.1016/j.jfda.2016.11.015. Epub 2017 Feb 16.
The present study investigated the regulatory effects of fish oil and chitosan on the signals of hepatic lipid metabolism and the postulated mechanism in high-fat diet-induced obese rats. Diet supplementation of chitosan and fish oil efficiently suppressed the increased weights in body and livers of high-fat diet-fed rats. Supplementation of chitosan and fish oil significantly decreased the activities of hepatic lipid biosynthesis-related enzymes and efficiently regulated plasma lipoprotein homeostasis. Both chitosan and fish oil significantly ameliorated the alterations in the protein expressions of hepatic lipogenic transcription factors (LXRα and PPARα), and could also significantly regulate the downstream hepatic lipogenic genes (FAS, HMGCR, CYP7A1, FATP, FABP, AOX, and ABCA) expressions in high-fat diet-fed rats. These results suggest that both fish oil and chitosan exerts downregulative effects on hepatic lipid metabolism in high-fat diet-induced obese rats via the LXRα inhibition and PPARα activation, which further affect the expressions of hepatic lipogenesis-associated genes.
本研究探讨了鱼油和壳聚糖对高脂饮食诱导肥胖大鼠肝脏脂质代谢信号的调节作用及其可能的机制。壳聚糖和鱼油的饮食补充有效地抑制了高脂饮食喂养大鼠体重和肝脏重量的增加。壳聚糖和鱼油的补充显著降低了肝脏脂质生物合成相关酶的活性,并有效地调节了血浆脂蛋白的动态平衡。壳聚糖和鱼油均显著改善了高脂饮食喂养大鼠肝脏生脂转录因子(LXRα和 PPARα)的蛋白表达改变,并能显著调节下游肝脏生脂基因(FAS、HMGCR、CYP7A1、FATP、FABP、AOX 和 ABCA)的表达。这些结果表明,鱼油和壳聚糖通过抑制 LXRα 和激活 PPARα,对高脂饮食诱导肥胖大鼠的肝脏脂质代谢发挥下调作用,进而影响肝脏生脂相关基因的表达。