虾肝肠胞虫感染凡纳滨对虾的脂质代谢变化特征

梁正; 贺洁; 张旋; 周颖; 童桂香; 谭红连; 马荣荣

doi:10.13300/j.cnki.hnlkxb.2026.03.026

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虾肝肠胞虫感染凡纳滨对虾的脂质代谢变化特征

动物科学·动物医学 | 更新时间：2026-11-05

- 虾肝肠胞虫感染凡纳滨对虾的脂质代谢变化特征
- Characterization of lipid metabolic alterations in Litopenaeus vannamei infected with Enterocytozoon hepatopenaei （EHP）
- 华中农业大学学报 2026年45卷第3期页码：282-291
- 作者机构：
  
  1.农业农村部中国（广西）-东盟水产种质资源综合开发与利用重点实验室（部省共建）/广西水产遗传育种与健康养殖重点实验室/广西壮族自治区水产科学研究院，南宁 530021
  2.台州市水产技术推广总站，台州 318000
  3.宁波大学海洋学院，宁波 315211
- 作者简介：
  
  梁正，E-mail：247708905@qq.com
  马荣荣，E-mail：marongrong@nbu.edu.cn
- 基金信息：
  
  广西壮族自治区水产科学研究院重点实验室开放课题(GXKEYLA-2023-02-2);台州市水产技术推广总站课题(24YY02)
- DOI：10.13300/j.cnki.hnlkxb.2026.03.026
  中图分类号： Q959.223⁺.63;S941.5
- 收稿：2025-07-25，
  
  纸质出版：2026-05-25
- 稿件说明：
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梁正，贺洁，张旋，等.虾肝肠胞虫感染凡纳滨对虾的脂质代谢变化特征［J］.华中农业大学学报，2026，45（3）：282‐291.

LIANG Zheng,HE Jie,ZHANG Xuan,et al.Characterization of lipid metabolic alterations in Litopenaeus vannamei infected with Enterocytozoon hepatopenaei （EHP）[J].Journal of Huazhong Agricultural University,2026,45(03):282-291.
梁正，贺洁，张旋，等.虾肝肠胞虫感染凡纳滨对虾的脂质代谢变化特征［J］.华中农业大学学报，2026，45（3）：282‐291. DOI： 10.13300/j.cnki.hnlkxb.2026.03.026.

LIANG Zheng,HE Jie,ZHANG Xuan,et al.Characterization of lipid metabolic alterations in Litopenaeus vannamei infected with Enterocytozoon hepatopenaei （EHP）[J].Journal of Huazhong Agricultural University,2026,45(03):282-291. DOI： 10.13300/j.cnki.hnlkxb.2026.03.026.

摘要

为解析虾肝肠胞虫（

Enterocytozoon hepatopenaei，

EHP）影响宿主能量代谢并造成宿主生长受阻的相关致病机制，从EHP慢性感染凡纳滨对虾的肝胰腺出发，综合运用透射电镜、组织病理学染色（油红O）、生化指标检测、荧光定量PCR（RT-qPCR）及高效液相色谱（HPLC）等技术，系统分析EHP感染过程中肝胰腺脂质积累、关键代谢酶活性、脂代谢相关基因表达及脂肪酸组成的变化。电镜结果显示EHP感染组的肝胰腺细胞间质内有许多大小不一的脂滴。油红O染色发现，EHP感染2周的对虾肝胰腺组织内出现明显的脂滴聚集。相关生化指标检测发现，感染初期（2周）甘油三酯（TG）含量显著升高，总胆固醇（T-CHO）含量在感染过程中与对照组变化趋势相似。此外，在感染的第3周和第4周，感染组对虾肝胰腺中脂蛋白脂肪酶（LPL）活性较对照组显著下降，而肝脂肪酶（HL）活性代偿性上升。RT-qPCR分析脂质代谢基因表达量发现，脂肪合成相关基因（

FAS、ACC

）显著上调，而脂肪分解代谢相关基因（

CPT1

、

AMPKα

、

ACDVL

、

ACDM

、

ACBP

、

ACDS

）明显下调，抑制脂肪酸β氧化。高效液相色谱技术测定结果显示，总脂肪酸含量相对于对照组显著下降（

0.05），但长链多不饱和脂肪酸（ARA、EPA、DHA）比例升高。以上结果表明，EHP通过干扰凡纳滨对虾脂质合成与脂肪酸分解，影响其体内的能量代谢循环。推测脂质代谢重塑是EHP慢性感染导致凡纳滨对虾生长受阻的重要病理变化之一。

Abstract

To elucidate the pathogenic mechanism by which

Enterocytozoon hepatopenaei

（EHP） affects host energy metabolism and causes growth retardation，this study focused on the hepatopancreas of

Litopenaeus vannamei

with chronic EHP infection.A comprehensive approach was employed utilizing techniques such as transmission electron microscopy，histopathological staining （Oil Red O），biochemical index assays，fluorescence quantitative PCR （RT-qPCR），and high-performance liquid chromatography （HPLC） to systematically analyze changes in lipid accumulation，key metabolic e

nzyme activities，expression of lipid metabolism-related genes，and fatty acid composition in the hepatopancreas during infection.Electron microscopy results revealed numerous lipid droplets of varying sizes in the interstitium of hepatopancreas cells in the EHP-infected group.Histological analysis showed obvious aggregation of lipid droplets in the hepatopancreas tissue of prawns infected with EHP for 2 weeks.Biochemical assays indicated a significant increase in triglyceride （TG） content during the early stage of infection （2 weeks），while total cholesterol （T-CHO） levels exhibited a trend similar to that of the control group during the infection process.In addition，in the 3rd and 4th weeks of infection，lipoprotein lipase （LPL） activity in the hepatopancreas of infected prawns decreased significantly compared to controls，whereas hepatic lipase （HL） activity increased compensatorily.RT-qPCR analysis of lipid metabolism gene expression showed that genes associated with fat synthesis （

FAS

，

ACC

） were significantly upregulated，while genes involved in fatty acid catabolism （

CPT1

，

AMPKα

，

ACDVL

，

ACDM

，

ACBP

，

ACDS

） were significantly downregulated，thereby inhibiting fatty acid β-oxidation.High-performance liquid chromatography results showed a significant decrease in total fatty acid content decreased significantly compared to the control group （

0.05），while the proportion of long-chain polyunsaturated fatty acids （ARA，EPA，DHA） increased.The above results indicate that EHP disrupts the energy metabolism cycle in

L.vannamei

by interfering with lipid synthesis and fatty acid degradation.This study demonstrates that lipid metabolism remodeling is an important pathological mechanism underlying growth retardation in

L.vannamei

caused by chronic EHP infection，providing a theoretical foundation for the prevention and control of EHP disease.

关键词

Keywords

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