scholarly journals Classification of the multigene family of fatty acid binding proteins (FABPs) and transcription profile of the genes in striped catfish (Pangasianodon hypophthalmus)

2021 ◽  
Vol 19 (2) ◽  
pp. 259-270
Author(s):  
Le Thi Nguyen Binh ◽  
Tran Son Hoang ◽  
Tran Thi Huyen Trang ◽  
Nguyen Thi Hoa ◽  
Kim Thi Phuong Oanh

Striped catfish (Pangasianodon hypophthalmus) is an economically important fish in Vietnam. The catfish fillets contain high fatty acid composition. The FABP family is involved in lipid transport and metabolism as well as in the regulation of gene expression and cell development. In this study, the catfish genome database was searched for fabp gene family; then, gene structure, classification and phylogenetic relationships were analyzed. In striped catfish genome, we found 10 fabp genes that are homologous to other fish species and other 5 novel fabp genes that have not been clearly annotated. These newly identified fabp genes cluster separately from the known members of the fabp family on the phylogenetic tree, and further studies are needed to understand their roles and functions. We examined transcriptional gene expression of fabp3, fabp7 and fabp10a genes in muscle, liver and brain tissues of the stripped catfish. The results showed that fabp10a gene was not strongly expressed in all 3 types of tissues; fabp3 gene was most strongly expressed in liver tissue and fabp7 was highly up-regulated in brain tissue. The results of this study provide a resource for further research on the function of fabp genes and their genetic diversity in striped catfish.

2021 ◽  
Author(s):  
Giovan N. Cholico ◽  
Russ R. Fling ◽  
Nicholas A. Zacharewski ◽  
Kelly A. Fader ◽  
Rance Nault ◽  
...  

ABSTRACT2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, induces steatosis by increasing hepatic uptake of dietary and mobilized peripheral fats, inhibiting lipoprotein export, and repressing β-oxidation. In this study, the mechanism of β-oxidation inhibition was investigated by testing the hypothesis that TCDD dose-dependently repressed straight-chain fatty acid oxidation gene expression in mice following oral gavage every 4 days for 28 days. Untargeted metabolomic analysis revealed a dose-dependent decrease in hepatic acyl-CoA levels, while octenoyl-CoA and dicarboxylic acid levels increased. TCDD also dose-dependently repressed the hepatic gene expression associated with triacylglycerol and cholesterol ester hydrolysis, fatty acid binding proteins, fatty acid activation, and 3-ketoacyl-CoA thiolysis while inducing acyl-CoA hydrolysis. Moreover, octenoyl-CoA blocked the hydration of crotonyl-CoA suggesting short chain enoyl-CoA hydratase (ECHS1) activity was inhibited. Collectively, the integration of metabolomics and RNA-seq data suggested TCDD induced a futile cycle of fatty acid activation and acyl-CoA hydrolysis resulting in incomplete β-oxidation, and the accumulation octenoyl-CoA levels that inhibited the activity of short chain enoyl-CoA hydratase (ECHS1).


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Giovan N. Cholico ◽  
Russell R. Fling ◽  
Nicholas A. Zacharewski ◽  
Kelly A. Fader ◽  
Rance Nault ◽  
...  

Abstract2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, induces steatosis by increasing hepatic uptake of dietary and mobilized peripheral fats, inhibiting lipoprotein export, and repressing β-oxidation. In this study, the mechanism of β-oxidation inhibition was investigated by testing the hypothesis that TCDD dose-dependently repressed straight-chain fatty acid oxidation gene expression in mice following oral gavage every 4 days for 28 days. Untargeted metabolomic analysis revealed a dose-dependent decrease in hepatic acyl-CoA levels, while octenoyl-CoA and dicarboxylic acid levels increased. TCDD also dose-dependently repressed the hepatic gene expression associated with triacylglycerol and cholesterol ester hydrolysis, fatty acid binding proteins, fatty acid activation, and 3-ketoacyl-CoA thiolysis while inducing acyl-CoA hydrolysis. Moreover, octenoyl-CoA blocked the hydration of crotonyl-CoA suggesting short chain enoyl-CoA hydratase (ECHS1) activity was inhibited. Collectively, the integration of metabolomics and RNA-seq data suggested TCDD induced a futile cycle of fatty acid activation and acyl-CoA hydrolysis resulting in incomplete β-oxidation, and the accumulation octenoyl-CoA levels that inhibited the activity of short chain enoyl-CoA hydratase (ECHS1).


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