Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets
An 8-week feeding trial was conducted, where turbot were fed four experimental diets, containing different LPC levels (0%, 0.1%, 0.25%, and 0.5%, named LPC0, LPC0.1, LPC0.25, and LPC0.5, respectively). The intestinal morphology results showed that there were no widened lamina propria and mixed infla...
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MDPI AG
2022-10-01
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author | Sihui Li Xing Luo Zhangbin Liao Mengqing Liang Houguo Xu Kangsen Mai Yanjiao Zhang |
author_facet | Sihui Li Xing Luo Zhangbin Liao Mengqing Liang Houguo Xu Kangsen Mai Yanjiao Zhang |
author_sort | Sihui Li |
collection | DOAJ |
description | An 8-week feeding trial was conducted, where turbot were fed four experimental diets, containing different LPC levels (0%, 0.1%, 0.25%, and 0.5%, named LPC0, LPC0.1, LPC0.25, and LPC0.5, respectively). The intestinal morphology results showed that there were no widened lamina propria and mixed inflammatory cells in the LPC-supplemented groups. Dietary LPC remarkably decreased the expression of TLRs (TLR3, TLR8, TLR9, and TLR22), MyD88, and signaling molecules (NF-κB, JNK, and AP-1). Similarly, diets with LPC supplementation markedly depressed the gene expression of NF-κB and JNK signaling pathway downstream genes (TNF-α, IL-1β, Bax, Caspase9, and Caspase-3). Furthermore, dietary LPC modified the intestinal microbial profiles, increasing the relative abundance of short-chain fatty acids-producers, lactic acid bacteria, and digestive enzyme-producing bacteria. Predictive functions of intestinal microbiota showed that turbot fed LPC diets had a relatively higher abundance of functions, such as lipid metabolism and immune system, but a lower abundance of functions, such as metabolic diseases and immune system diseases. The activities of intestinal acid phosphatase and alkaline phosphatase were also increased by dietary LPC. In conclusion, LPC supplementation could regulate the intestinal mucosal barrier via the TLR signaling pathway and alter the intestinal microbiota profile of turbot fed high-lipid diets. |
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last_indexed | 2024-03-09T19:39:03Z |
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spelling | doaj.art-fcc5360313784ccd8e79ad750bb5ee9a2023-11-24T01:46:05ZengMDPI AGNutrients2072-66432022-10-011420439810.3390/nu14204398Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid DietsSihui Li0Xing Luo1Zhangbin Liao2Mengqing Liang3Houguo Xu4Kangsen Mai5Yanjiao Zhang6The Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture), The Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, 5 Yushan Road, Qingdao 266003, ChinaYellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, 106 Nanjing Road, Qingdao 266071, ChinaYellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, 106 Nanjing Road, Qingdao 266071, ChinaYellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, 106 Nanjing Road, Qingdao 266071, ChinaYellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, 106 Nanjing Road, Qingdao 266071, ChinaThe Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture), The Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, 5 Yushan Road, Qingdao 266003, ChinaThe Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture), The Key Laboratory of Mariculture (Ministry of Education), Ocean University of China, 5 Yushan Road, Qingdao 266003, ChinaAn 8-week feeding trial was conducted, where turbot were fed four experimental diets, containing different LPC levels (0%, 0.1%, 0.25%, and 0.5%, named LPC0, LPC0.1, LPC0.25, and LPC0.5, respectively). The intestinal morphology results showed that there were no widened lamina propria and mixed inflammatory cells in the LPC-supplemented groups. Dietary LPC remarkably decreased the expression of TLRs (TLR3, TLR8, TLR9, and TLR22), MyD88, and signaling molecules (NF-κB, JNK, and AP-1). Similarly, diets with LPC supplementation markedly depressed the gene expression of NF-κB and JNK signaling pathway downstream genes (TNF-α, IL-1β, Bax, Caspase9, and Caspase-3). Furthermore, dietary LPC modified the intestinal microbial profiles, increasing the relative abundance of short-chain fatty acids-producers, lactic acid bacteria, and digestive enzyme-producing bacteria. Predictive functions of intestinal microbiota showed that turbot fed LPC diets had a relatively higher abundance of functions, such as lipid metabolism and immune system, but a lower abundance of functions, such as metabolic diseases and immune system diseases. The activities of intestinal acid phosphatase and alkaline phosphatase were also increased by dietary LPC. In conclusion, LPC supplementation could regulate the intestinal mucosal barrier via the TLR signaling pathway and alter the intestinal microbiota profile of turbot fed high-lipid diets.https://www.mdpi.com/2072-6643/14/20/4398lysophospholipidintestinal histological analysisToll-like receptorpro-inflammatory cytokinesapoptosisintestinal mucosal barrier |
spellingShingle | Sihui Li Xing Luo Zhangbin Liao Mengqing Liang Houguo Xu Kangsen Mai Yanjiao Zhang Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets Nutrients lysophospholipid intestinal histological analysis Toll-like receptor pro-inflammatory cytokines apoptosis intestinal mucosal barrier |
title | Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets |
title_full | Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets |
title_fullStr | Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets |
title_full_unstemmed | Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets |
title_short | Effects of Lysophosphatidylcholine on Intestinal Health of Turbot Fed High-Lipid Diets |
title_sort | effects of lysophosphatidylcholine on intestinal health of turbot fed high lipid diets |
topic | lysophospholipid intestinal histological analysis Toll-like receptor pro-inflammatory cytokines apoptosis intestinal mucosal barrier |
url | https://www.mdpi.com/2072-6643/14/20/4398 |
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