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肠道蠕虫(山口,1934年)感染通过免疫和肠道微生物群调节改善草鱼的脂质代谢。

Intestinal helminth Yamaguti, 1934 infection ameliorate lipid metabolism of grass carp () through immune and gut microbiota regulation.

作者信息

Yang Xiaoao, Zhu Denghui, Li Wenxiang, Fu Peipei

机构信息

National Engineering Research Center of Marine Facilities Aquaculture, Marine Science and Technology College, Zhejiang Ocean University, Zhoushan, China.

National Engineering Laboratory of Marine Germplasm Resources Exploration and Utilization, Marine Science and Technology College, Zhejiang Ocean University, Zhoushan, China.

出版信息

Front Microbiol. 2025 Jul 10;16:1538919. doi: 10.3389/fmicb.2025.1538919. eCollection 2025.

DOI:10.3389/fmicb.2025.1538919
PMID:40708918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12287012/
Abstract

Fats have been widely applied in aquaculture to promote growth performance and substitute partial protein in fish feeds. However, excessive dietary fat levels induce metabolic disorders harming the health of cultured fish. Helminth infection in mammals was inversely correlated with metabolic syndrome, but its effect in aquatic animals is unknown yet. Here, we evaluated the impacts of infection on lipid metabolism of grass carp fed with high-fat diet (HFD). By comparison with the uninfected grass carp, helminth infection significantly increased the concentration of high-density lipoprotein (HDL) and condition factor (CF), and significantly decreased the concentration of low-density lipoprotein (LDL), the activity of AST, perimeter ratio (PR) and the thickness of muscularis mucosa (MM). Helminth infection also significantly lowered the lipid accumulation in liver, which may attribute to the significant up-regulated expression levels of apolipoprotein E () and down-regulated expression of peroxisome proliferator-activated receptor-gamma (γ) and lipoprotein lipase (). Meanwhile in the grass carp infected by tapeworm, there was significant down-regulated expression of pro-inflammatory genes, interleukin-1beta (β) and tumor necrosis factor-alpha (α), and significant up-regulated expression of anti-inflammatory genes, transforming growth factor-beta 1 (β) and interleukin-10 (). 16S rDNA sequencing results showed that helminth infection didn't affect the α diversity of the intestinal microbiota, but increased the relative abundance of , and significantly changed the structure of intestinal microbiota by PERMANOVA analysis. Correlation analysis showed the relative abundance of was significant positively correlated with the helminth infection in grass carp fed HFD. PICRUST2 analysis indicated that several lipid metabolism-related pathways were significantly altered after helminth infection. Consequently, the above results indicated that tapeworm infection could ameliorate abnormal lipid metabolism through immune and gut microbiota regulation.

摘要

脂肪已广泛应用于水产养殖,以促进生长性能并替代鱼饲料中的部分蛋白质。然而,过高的日粮脂肪水平会引发代谢紊乱,损害养殖鱼类的健康。哺乳动物中的蠕虫感染与代谢综合征呈负相关,但其在水生动物中的作用尚不清楚。在此,我们评估了感染对高脂饮食(HFD)喂养的草鱼脂质代谢的影响。与未感染的草鱼相比,蠕虫感染显著提高了高密度脂蛋白(HDL)浓度和肥满度(CF),并显著降低了低密度脂蛋白(LDL)浓度、谷草转氨酶(AST)活性、周径比(PR)和黏膜肌层厚度(MM)。蠕虫感染还显著降低了肝脏中的脂质积累,这可能归因于载脂蛋白E()表达水平的显著上调以及过氧化物酶体增殖物激活受体γ(γ)和脂蛋白脂肪酶()表达的下调。同时,在感染绦虫的草鱼中,促炎基因白细胞介素-1β(β)和肿瘤坏死因子-α(α)的表达显著下调,抗炎基因转化生长因子-β1(β)和白细胞介素-10()的表达显著上调。16S rDNA测序结果表明,蠕虫感染不影响肠道微生物群的α多样性,但增加了的相对丰度,并且通过PERMANOVA分析显著改变了肠道微生物群的结构。相关性分析表明,在高脂饮食喂养的草鱼中,的相对丰度与蠕虫感染呈显著正相关。PICRUST2分析表明,蠕虫感染后,几个与脂质代谢相关的途径发生了显著改变。因此,上述结果表明,绦虫感染可通过免疫和肠道微生物群调节改善异常脂质代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/abe781f5c26e/fmicb-16-1538919-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/5d15ca281392/fmicb-16-1538919-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/1e5687b68e55/fmicb-16-1538919-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/2c0f6f574695/fmicb-16-1538919-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/05da4638198b/fmicb-16-1538919-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/abe781f5c26e/fmicb-16-1538919-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/5d15ca281392/fmicb-16-1538919-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/1e5687b68e55/fmicb-16-1538919-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/2c0f6f574695/fmicb-16-1538919-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/05da4638198b/fmicb-16-1538919-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2f/12287012/abe781f5c26e/fmicb-16-1538919-g005.jpg

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