Introduction: Lipid accumulation in the liver can negatively impact liver function and health, which is well-described for humans and other mammals, but relatively unexplored in Atlantic salmon. This study investigates the phenotypic, genetic, and transcriptomic variations related to individual differences in liver fat content within a group of slaughter-sized Atlantic salmon reared under the same conditions and fed the same feed. The objective was to increase the knowledge on liver fat deposition in farmed salmon and evaluate the potential for genetic improvement of this trait.
Methods: The study involved measuring liver fat content in a group of slaughter-sized Atlantic salmon. Genetic analysis included estimating heritability and conducting genome-wide association studies (GWAS) to identify quantitative trait loci (QTLs). Transcriptomic analysis was performed to link liver fat content to gene expression, focusing on genes involved in lipid metabolic processes.
Results: There was a large variation in liver fat content, ranging from 3.6% to 18.8%, with frequent occurrences of high liver fat. Livers with higher levels of fat had higher proportions of the fatty acids 16:1 n-7, 18:2 n-6, and 18:1 n-9, and less of the long-chain omega-3 fatty acids. The heritability of liver fat was estimated at 0.38, and the genetic coefficient of variation was 20%, indicating substantial potential for selective breeding to reduce liver fat deposition in Atlantic salmon. Liver fat deposition appears to be a polygenic trait, with no large QTLs detected by GWAS. Gene expression analysis linked liver fat content to numerous genes involved in lipid metabolic processes, including key transcription factors such as LXR, SREBP1, and ChREBP.
Discussion: The results indicated a connection between liver fat and increased cholesterol synthesis in Atlantic salmon, with potentially harmful free cholesterol accumulation. Further, the gene expression results linked liver fat accumulation to reduced peroxisomal β-oxidation, increased conversion of carbohydrates to lipids, altered phospholipid synthesis, and possibly increased lipogenesis. It is undetermined whether these outcomes are due to high fat levels or if they are caused by underlying metabolic differences that result in higher liver fat levels in certain individuals. Nonetheless, the results provide new insights into the metabolic profile of livers in fish with inherent differences in liver fat content.
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http://dx.doi.org/10.3389/fgene.2025.1512769 | DOI Listing |
Dig Liver Dis
March 2025
Gastroenterology Unit, Nazareth Hospital EMMS, Azrieli Faculty of Medicine, Bar Ilan University, Ramat Gan, Israel. Electronic address:
Environ Health Prev Med
March 2025
Department of Gastroenterology, Hematology and Clinical Immunology, Hirosaki University Graduate School of Medicine.
Background: Many factors are associated with the development and progression of liver fat and fibrosis; however, genetics and the gut microbiota are representative factors. Moreover, recent studies have indicated a link between host genes and the gut microbiota. This study investigated the effect of patatin-like phospholipase domain-containing 3 (PNPLA3) rs738409 (C > G), which has been reported to be most involved in the onset and progression of fatty liver, on liver fat and fibrosis in a cohort study related to gut microbiota in a non-fatty liver population.
View Article and Find Full Text PDFLife Sci
March 2025
Hepatopancreatobiliary Center, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua Medicine of Tsinghua University, Beijing 102218, China; Ministry of Education Key Laboratory of Digital Intelligence Hepatology, Tsinghua University, Beijing 100084, China. Electronic address:
Aims: This study investigates the potential of Bifidobacterium bifidum 1,007,478 (BB478) and its metabolite indole-3-lactic acid (ILA) in alleviating non-alcoholic steatohepatitis (NASH) induced by a high-fat diet (HFD) and fructose exposure.
Materials And Methods: A zebrafish model of NASH was established by exposure to HFD and fructose. BB478 was administered, and the effects on liver lipid accumulation, oxidative stress, and inflammation were assessed.
Int J Biol Macromol
March 2025
Department of Liver Transplant, The Second Xiangya Hospital of Central South University, 410011 Changsha, China. Electronic address:
Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic condition with an incompletely understood pathogenesis. In this study, five candidate genes-RAG1, CKAP2, CENPK, TYMS, and BUB1-were identified as being associated with NAFLD progression through integrative bioinformatics analyses. A predictive model incorporating these genes demonstrated strong robustness and diagnostic accuracy.
View Article and Find Full Text PDFProg Lipid Res
March 2025
Department of Biochemistry, Kagawa University School of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan. Electronic address:
The phospholipase A and acyltransferase (PLAAT) family is a group of structurally related proteins that are conserved among vertebrates. In humans, the family comprises five members (PLAAT1-5), which share common domain structures, and functions as phospholipase A/A and acyltransferase enzymes. Regarding acyltransferase activities, PLAATs produce N-acyl-phosphatidylethanolamines, which serve as the precursor of bioactive N-acylethanolamines (NAEs).
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