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日粮补充胆汁酸可减少肉鸡肝脏脂肪沉积,这与肠道微生物群和肝脏胆汁酸谱的改变有关。

Dietary bile acids supplementation decreases hepatic fat deposition with the involvement of altered gut microbiota and liver bile acids profile in broiler chickens.

作者信息

Wang Minghui, Li Kelin, Jiao Hongchao, Zhao Jingpeng, Li Haifang, Zhou Yunlei, Cao Aizhi, Wang Jianmin, Wang Xiaojuan, Lin Hai

机构信息

College of Animal Science and Technology, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Key Laboratory of Efficient Utilization of Non-Grain Feed Resources (Co-Construction By Ministry and Province), Ministry of Agriculture and Rural Affairs, Shandong Agricultural University, No. 61, Daizong Street, Taian, 271018, Shandong, P. R. China.

College of Life Sciences, Shandong Agricultural University, No. 61, Daizong Street, Taian, 271018, Shandong, P. R. China.

出版信息

J Anim Sci Biotechnol. 2024 Aug 13;15(1):113. doi: 10.1186/s40104-024-01071-y.

DOI:10.1186/s40104-024-01071-y
PMID:39135090
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11320850/
Abstract

BACKGROUND

High-fat diets (HFD) are known to enhance feed conversion ratio in broiler chickens, yet they can also result in hepatic fat accumulation. Bile acids (BAs) and gut microbiota also play key roles in the formation of fatty liver. In this study, our objective was to elucidate the mechanisms through which BA supplementation reduces hepatic fat deposition in broiler chickens, with a focus on the involvement of gut microbiota and liver BA composition.

RESULTS

Newly hatched broiler chickens were allocated to either a low-fat diet (LFD) or HFD, supplemented with or without BAs, and subsequently assessed their impacts on gut microbiota, hepatic lipid metabolism, and hepatic BA composition. Our findings showed that BA supplementation significantly reduced plasma and liver tissue triglyceride (TG) levels in 42-day-old broiler chickens (P < 0.05), concurrently with a significant decrease in the expression levels of fatty acid synthase (FAS) in liver tissue (P < 0.05). These results suggest that BA supplementation effectively diminishes hepatic fat deposition. Under the LFD, BAs supplementation increased the BA content and ratio of Non 12-OH BAs/12-OH BAs in the liver and increased the Akkermansia abundance in cecum. Under the HFD, BA supplementation decreased the BAs and increased the relative abundances of chenodeoxycholic acid (CDCA) and cholic acid (CA) in hepatic tissue, while the relative abundances of Bacteroides were dramatically reduced and the Bifidobacterium, Escherichia, and Lactobacillus were increased in cecum. Correlation analyses showed a significant positive correlation between the Akkermansia abundance and Non 12-OH BA content under the LFD, and presented a significant negative correlation between the Bacteroides abundance and CA or CDCA content under the HFD.

CONCLUSIONS

The results indicate that supplementation of BAs in both LFD and HFD may ameliorate hepatic fat deposition in broiler chickens with the involvement of differentiated microbiota-bile acid profile pathways.

摘要

背景

已知高脂饮食(HFD)可提高肉鸡的饲料转化率,但也会导致肝脏脂肪堆积。胆汁酸(BAs)和肠道微生物群在脂肪肝的形成中也起着关键作用。在本研究中,我们的目的是阐明补充胆汁酸减少肉鸡肝脏脂肪沉积的机制,重点关注肠道微生物群和肝脏胆汁酸组成的参与情况。

结果

将新孵化的肉鸡分为低脂饮食(LFD)或高脂饮食组,分别补充或不补充胆汁酸,随后评估其对肠道微生物群、肝脏脂质代谢和肝脏胆汁酸组成的影响。我们的研究结果表明,补充胆汁酸可显著降低42日龄肉鸡的血浆和肝脏组织甘油三酯(TG)水平(P < 0.05),同时肝脏组织中脂肪酸合酶(FAS)的表达水平显著降低(P < 0.05)。这些结果表明,补充胆汁酸可有效减少肝脏脂肪沉积。在低脂饮食条件下,补充胆汁酸可增加肝脏中胆汁酸含量以及非12-OH BAs/12-OH BAs的比例,并增加盲肠中阿克曼氏菌的丰度。在高脂饮食条件下,补充胆汁酸可降低肝脏中胆汁酸含量,并增加鹅去氧胆酸(CDCA)和胆酸(CA)的相对丰度,而盲肠中拟杆菌的相对丰度显著降低,并增加了双歧杆菌、大肠杆菌和乳酸杆菌的丰度。相关性分析表明,在低脂饮食条件下,阿克曼氏菌丰度与非12-OH BA含量之间存在显著正相关,而在高脂饮食条件下,拟杆菌丰度与CA或CDCA含量之间存在显著负相关。

结论

结果表明低脂和高脂饮食中补充胆汁酸可能通过不同的微生物群-胆汁酸谱途径改善肉鸡肝脏脂肪沉积。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/b6f02daed875/40104_2024_1071_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/914cd7202042/40104_2024_1071_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/b6f02daed875/40104_2024_1071_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/4c722b4526eb/40104_2024_1071_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/6ff3362b57c7/40104_2024_1071_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/4b275cf6eb96/40104_2024_1071_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/c938bd023d42/40104_2024_1071_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/46f8d29a7a25/40104_2024_1071_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/12399217fb17/40104_2024_1071_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/914cd7202042/40104_2024_1071_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec91/11320850/b6f02daed875/40104_2024_1071_Fig9_HTML.jpg

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