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This experiment was conducted to investigate whether dietary chenodeoxycholic acid (CDCA) could attenuate high-fat (HF) diet-induced growth retardation, lipid accumulation and bile acid (BA) metabolism disorder in the liver of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (initial weight: 4·40 (sem 0·08) g) were fed four diets: the control (105·8 g/kg lipid), HF diet (HF group, 159·6 g/kg lipid), the control supplemented with 0·9 g/kg CDCA (CDCA group) and HF diet supplemented with 0·9 g/kg CDCA (HF + CDCA group). CDCA supplemented in the HF diet significantly improved growth performance and feed utilisation of yellow catfish (P < 0·05). CDCA alleviated HF-induced increment of hepatic lipid and cholesterol contents by down-regulating the expressions of lipogenesis-related genes and proteins and up-regulating the expressions of lipololysis-related genes and proteins. Compared with the control group, CDCA group significantly reduced cholesterol level (P < 0·05). CDCA significantly inhibited BA biosynthesis and changed BA profile by activating farnesoid X receptor (P < 0·05). The contents of CDCA, taurochenodeoxycholic acid and glycochenodeoxycholic acid were significantly increased with the supplementation of CDCA (P < 0·05). HF-induced elevation of cholic acid content was significantly attenuated by the supplementation of CDCA (P < 0·05). Supplementation of CDCA in the control and HF groups could improve the liver antioxidant capacity. This study proved that CDCA could improve growth retardation, lipid accumulation and BA metabolism disorder induced by HF diet, which provided new insight into understanding the physiological functions of BA in fish. [ABSTRACT FROM AUTHOR]

Aims: Studies demonstrated that oxidized fish oil (OFO) promoted oxidative stress and induced mitochondrial dysfunction and lipotoxicity, which attenuated beneficial effects of fish oil supplements in the treatment of nonalcoholic fatty liver disease (NAFLD). The current study was performed on yellow catfish, a good model to study NAFLD, and its hepatocytes to explore whether selenium (Se) could alleviate OFO-induced lipotoxicity via the inhibition of oxidative stress and determine its potential mechanism. Results: The analysis of triglycerides content, oxidative stress parameters, and histological and transmission electronic microscopy observation showed that high dietary Se supplementation alleviated OFO-induced lipotoxicity, oxidative stress, and mitochondrial injury and dysfunction. RNA-sequencing and immunoblotting analysis indicated that high dietary Se reduced OFO-induced decline of peroxisome-proliferator-activated receptor alpha (Pparα) and ubiquitin-specific protease 4 (Usp4) protein expression. High Se supplementation also alleviated OFO-induced reduction of thioredoxin reductase 2 (txnrd2) messenger RNA (mRNA) expression level and activity. The txnrd2 knockdown experiments revealed that txnrd2 mediated Se- and oxidized eicosapentaenoic acid (oxEPA)-induced changes of mitochondrial reactive oxygen species (mtROS) and further altered Usp4 mediated-deubiquitination and stabilization of Pparα, which, in turn, modulated mitochondrial fatty acid β-oxidation and metabolism. Mechanistically, Usp4 deubiquitinated Pparα and ubiquitin-proteasome-mediated Pparα degradation contributed to oxidative stress-induced mitochondrial dysfunction. Innovation: These findings uncovered a previously unknown mechanism by which Se and OFO interacted to affect lipid metabolism via the Txnrd2-mtROS-Usp4-Pparα pathway, which provides the new target for NAFLD prevention and treatment. Conclusion: Se ameliorated OFO-induced lipotoxicity via the inhibition of mitochondrial oxidative stress, remodeling of Usp4-mediated deubiquitination, and stabilization of Pparα. Antioxid. Redox Signal. 40, 433–452. [ABSTRACT FROM AUTHOR]

The article focuses on dietary selenium sources differentially regulate selenium concentration, mRNA and protein expression of representative selenoproteins in various tissues of yellow catfish Pelteobagrus fulvidraco.

Nowadays, fatty liver and visceral excessive lipid accumulation are common in cultured fish, which reduces survival rate, growth performance and disease resistance. Yellow catfish Pelteobagrus fulvidraco is widely distributed in rivers, lakes and other fresh waters in China, and cultured in China and several Asian countries. The fish has relatively high economic value because of delicious taste and abundant nutrition. However, due to intensive culture and improper feeding, excessive fat accumulation in abdominal cavity and liver commonly occurs, which seriously affects the taste and health of yellow catfish. Therefore, the research on fat metabolism of yellow catfish has always been the focus. Lysosomal acid lipase (LAL), encoded by LIPA, hydrolyzes cholesterylesters (CEs) and triglycerides (TGs) to cholesterol and free fatty acids (FFAs), which are then used for metabolic purposes in the cells. The studies have been conducted to explore lal structure in mammals, but were scarce in fish. For this reason, it is important to study the molecular characteristics of lal in the regulation of lipid metabolism of yellow catfish. In this study, we analyzed molecular structure, tissue expression, promoter structure and function, and transcriptional regulation of lal. The lal gene was amplified from yellow catfish by RT-PCR and RACE approaches. The cDNAs of lal was 1802 bp, encoding a peptide of 398 amino acid residues, and 5' upstream promoter was 2052 bp in length. The molecular weight of the theoretical protein was 45.42 kDa, the isoelectric point was 7.70, and it had a signal peptide with 23 residues, five glycosylation sites, three cysteines, a catalytic ternary and a "cap" domain and a "lid" region. The amino acid alignment and phylogenetic analysis revealed that lal of P. fulvidraco was closely related to that of Ictalurus punctatus. The lal mRNA was expressed in all tested tissues (heart, liver, brain, spleen, kidney, muscle, fat, intestine, testis and ovary), with the highest expression levels in spleen, intestine and testis. Promoter sequence analysis revealed several transcription factor binding sites in lal promoter, such as Sp1, STAT3, PPARα, FOXO1, PPARγ, and HNF4α. Studies on promoter activity showed that -1507/-1016 region negatively regulated promoter activity, while -1016/+51 region positively regulated promoter activity. The present study indicated that lal mRNA was expressed in multiple high metabolism tissues. The transcription of lal was regulated by multiple transcription factors. This study help us to understand the structure and function of lal, and lay a foundation for further research on the regulatory mechanism of lipid metabolism in fish. [ABSTRACT FROM AUTHOR]