Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture and Rural Affairs) and Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, Qingdao, China.
Tongwei Co., Ltd., Chengdu, China.
Front Immunol. 2022 Aug 19;13:984508. doi: 10.3389/fimmu.2022.984508. eCollection 2022.
In the 21 century, intestinal homeostatic imbalance has emerged as a growing health challenge worldwide. Accumulating evidence reveals that excessive intake of saturated fatty acid (SFA) induces intestinal homeostatic imbalance. However, the potential molecular mechanism is still unclear. In the present study, we found that palm oil or palmitic acid (PA) treatment disturbed lipid metabolism homeostasis and triggered endoplasmic reticulum (ER) stress and inflammation in the intestine or intestinal cells of large yellow croaker (). Interestingly, PA treatment significantly decreased phosphatidylethanolamine (PE) content in the intestinal cells. PE supplementation decreased triglyceride content in the intestinal cells induced by PA treatment by inhibiting fatty acid uptake and lipogenesis. PE supplementation suppressed ER stress. Meanwhile, PE supplementation alleviated inflammatory response through p38 MAPK-p65 pathway, reducing the damage of intestinal cells caused by PA treatment to some extent. Our work revealed that intestinal homeostatic imbalance caused by PA treatment was partly due to the decrease of PE content. PE consumption might be a nutritional strategy to regulate intestinal homeostasis in fish and even human beings.
在 21 世纪，肠道内稳态失衡已成为全球范围内日益严重的健康挑战。越来越多的证据表明，饱和脂肪酸（SFA）的过度摄入会导致肠道内稳态失衡。然而，其潜在的分子机制尚不清楚。在本研究中，我们发现棕榈油或棕榈酸（PA）处理扰乱了脂质代谢的内稳态，并在大黄鱼的肠道或肠道细胞中引发内质网（ER）应激和炎症（）。有趣的是，PA 处理显著降低了肠道细胞中磷脂酰乙醇胺（PE）的含量。PE 补充通过抑制脂肪酸摄取和脂肪生成，降低了 PA 处理诱导的肠道细胞中甘油三酯的含量。PE 补充抑制了 ER 应激。同时，PE 补充通过 p38 MAPK-p65 通路减轻了炎症反应，从而在一定程度上减轻了 PA 处理对肠道细胞的损伤。我们的工作揭示了 PA 处理引起的肠道内稳态失衡部分归因于 PE 含量的降低。PE 的消耗可能是调节鱼类甚至人类肠道内稳态的一种营养策略。
