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猪空肠来源的细胞外囊泡参与脂质代谢的调节。

Porcine jejunal-derived extracellular vesicles participate in the regulation of lipid metabolism.

作者信息

Fan Yaotian, Deng Haibin, Zhu Jiahao, Luo Junyi, Chen Ting, Sun Jiajie, Zhang Yongliang, Xi Qianyun

机构信息

Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.

出版信息

J Anim Sci Biotechnol. 2025 Apr 7;16(1):53. doi: 10.1186/s40104-025-01185-x.

DOI:10.1186/s40104-025-01185-x
PMID:40189541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11974103/
Abstract

BACKGROUND

Regulating the regional deposition of fat is crucial for improving the carcass characteristics of pigs. The intestine, as an important organ for lipid absorption and homeostasis maintenance, secretes various biological signals that participate in the crosstalk between the intestine and adipose tissue. Extracellular vesicles, as novel extracellular genetic factors that mediate metabolic signal exchange among multiple tissues, have emerged as a hotspot and breakthrough in revealing the mechanisms of physiological homeostasis. However, how extracellular vesicles regulate the intestinal-adipose signaling axis, especially in relation lipid metabolism and deposition is still unclear. Thus, in the current study, intestinal extracellular vesicles from Chinese fat-type piglets of Lantang and typical lean-type piglets of Landrace were isolated and identified, and to reveal the regulatory mechanisms of lipid metabolism via intestinal extracellular vesicles in mediating intestinal-adipose crosstalk.

RESULTS

We isolated and identified intestinal extracellular vesicles from the jejunum of 3-day-old Lantang and Landrace piglets (LT-EVs and LD-EVs) and further investigated their effects on lipid accumulation in porcine primary adipocytes. Compared to LD-EVs, LT-EVs promoted lipid deposition in porcine primary adipocytes, with intestinal-derived miRNAs playing a critical role in the crosstalk between the intestine and adipose tissue. Further analysis of extracellular vesicles-derived miRNA sequencing revealed that miR-30b-5p, enriched in LD-EVs, is involved in the regulation of lipid metabolism. Notably, the enrichment of miR-30b-5p in extracellular vesicles derived from IPEC-J2 cells also influenced lipid metabolism. Mechanistically, the targeted binding of miR-30b-5p and FMO3 may be critical for the extracellular vesicle-mediated regulation of lipid metabolism.

CONCLUSIONS

Our findings suggest that jejunal-derived extracellular vesicles play a critical role in regulating lipid metabolism, and the regulatory effect of extracellular vesicles from obese piglets was higher than that of lean piglets. Furthermore, the different expression of miRNAs, such as miR-30b-5p, in intestinal extracellular vesicles may be the key to determining lipid deposition phenotypes across the two pig breeds.

摘要

背景

调节脂肪的区域沉积对于改善猪的胴体特性至关重要。肠道作为脂质吸收和体内稳态维持的重要器官,分泌多种参与肠道与脂肪组织间相互作用的生物信号。细胞外囊泡作为介导多种组织间代谢信号交换的新型细胞外遗传因子,已成为揭示生理稳态机制的热点和突破点。然而,细胞外囊泡如何调节肠 - 脂肪信号轴,特别是与脂质代谢和沉积相关的机制仍不清楚。因此,在本研究中,分离并鉴定了来自中国蓝塘脂肪型仔猪和长白典型瘦肉型仔猪的肠道细胞外囊泡,以揭示肠道细胞外囊泡在介导肠 - 脂肪相互作用中调节脂质代谢的机制。

结果

我们从3日龄蓝塘和长白仔猪的空肠中分离并鉴定了肠道细胞外囊泡(LT-EVs和LD-EVs),并进一步研究了它们对猪原代脂肪细胞脂质积累的影响。与LD-EVs相比,LT-EVs促进了猪原代脂肪细胞中的脂质沉积,肠道来源的miRNA在肠道与脂肪组织的相互作用中起关键作用。对细胞外囊泡衍生的miRNA测序的进一步分析表明,富集于LD-EVs中的miR-30b-5p参与脂质代谢的调节。值得注意的是,miR-30b-5p在IPEC-J2细胞衍生的细胞外囊泡中的富集也影响了脂质代谢。从机制上讲,miR-30b-5p与FMO3的靶向结合可能对细胞外囊泡介导的脂质代谢调节至关重要。

结论

我们的研究结果表明,空肠来源的细胞外囊泡在调节脂质代谢中起关键作用,肥胖仔猪的细胞外囊泡的调节作用高于瘦肉型仔猪。此外,肠道细胞外囊泡中miR-30b-5p等miRNA的不同表达可能是决定这两个猪品种脂质沉积表型的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/671c6c62f5da/40104_2025_1185_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/c60d34bbd5c3/40104_2025_1185_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/6b77f5bad20c/40104_2025_1185_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/74c7b6810b68/40104_2025_1185_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/7ee845945676/40104_2025_1185_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/671c6c62f5da/40104_2025_1185_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/c60d34bbd5c3/40104_2025_1185_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/6b77f5bad20c/40104_2025_1185_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/74c7b6810b68/40104_2025_1185_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/7ee845945676/40104_2025_1185_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93f4/11974103/671c6c62f5da/40104_2025_1185_Fig5_HTML.jpg

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