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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]

This study investigated the effects of dietary Se levels on lipid metabolism and miRNA expression in the mesenteric adipose tissue of yellow catfish. Three experimental diets were formulated to contain 0.03 (low Se), 0.25 (adequate Se, control) and 6.39 mg Se/kg (high Se) for a 12-week trial. The enzymatic activities of lipogenesis, the expression levels of miRNA and its target gene related to lipid metabolism were detected. Compared with the control group, TG content increased significantly in the high-selenium group and low selenium group (P<0.05). Compared with the control group, the enzyme activities of G6PD and 6PGD decreased significantly in the low Se group (P<0.05), and significantly increased in the high Se group (P<0.05). Compared with the control group, the enzyme activity of ICDH decreased significantly in the high-Se group (P<0.05) with no significant change in the low-Se group; the enzyme activities of ME and FAS both increased significantly in the low and high Se groups (P<0.05); the expression levels of mir- 26a, mir-183, mir-135, let-7b, let-7c and let-7g in the high Se group increased significantly (P<0.05) with no significant difference in the low Se group. Though mir-181a-5p and let-7e increased significantly in the low-selenium group (P<0.05), it showed no significant difference in the high-selenium group. Selenium significantly increased mir-130 and mir-203a (P<0.05). Low selenium decreased significantly but high selenium increased the expressions of miR-200a, miR-143, let-7d and let-7f (P<0.05). MiR-143, miR-203a and miR-130 were highly expressed in adipose tissue, which were strongly responded to dietary Se levels. We used TargetScanFish6.2 and miRwalk3.0 to predict target genes of miR-130, miR-203a and miR-143, and performed KEGG enrichment analysis of target genes. The target genes of miR- 143 enriched significantly in mineral absorption, unsaturated fatty acid biosynthesis and insulin pathway (P<0.05, FDR≤ 0.05). The target genes of miR-203a was significantly enriched in lipid metabolic pathways and insulin signaling pathways (P<0.05, FDR≤0.05). The target genes of miR-130 enriched significantly in sphingolipid metabolism, lipid accumulation and mTOR signaling pathway (P<0.05, FDR≤0.05). Comprehensive analysis found that miR-130, miR-143 and miR-203a target genes were enriched in fatty acid synthesis signaling pathway, autophagy, apoptosis and insulin resistance. Then we selected target genes that both enriched in these signaling pathways for qPCR. The fas, cpt1a, hsl, srebp1, pparα and atgl mRNA expressions was consistent with miR-143, miR-203a and miR-130 expression levels. Therefore, we speculated that the dietary Se induced lipid metabolism via miR-143-, miR-203a- and miR-130-mediated expressions of fas, cpt1a, hsl, srebp1, pparα and atgl. [ABSTRACT FROM AUTHOR]

The present study explored the mechanisms of dietary Zn influencing Zn and lipid deposition in the fore- and mid- intestine in yellow catfish Pelteobagrus fulvidraco, and investigated whether the mechanism was intestinal-region dependent. For this purpose, yellow catfish were fed three diets containing Zn levels of 8·83, 19·20 and 146·65 mg Zn/kg, respectively. Growth performance, intestinal TAG and Zn contents as well as activities and mRNA expression of enzymes and genes involved in Zn transport and lipid metabolism in the fore- and mid-intestine were analysed. Dietary Zn increased Zn accumulation as well as activities of Cu-, Zn-superoxide dismutase and ATPase in the fore- and mid-intestine. In the fore-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, metallothionein (MT) and metal response element-binding transcription factor-1 (MTF-1), but down-regulated mRNA levels of ZIP4 and ZIP5. In the mid-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, MT and MTF-1, but down-regulated mRNA levels of ZIP4 and ZIP5. Dietary Zn reduced TAG content, down-regulated activities of 6-phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME) and fatty acid synthase (FAS) activities, and reduced mRNA levels of 6PGD, G6PD, FAS, PPARγ and sterol-regulator element-binding protein (SREBP-1), but up-regulated mRNA levels of carnitine palmitoyltransferase IA, hormone-sensitive lipase (HSLa), adipose TAG lipase (ATGL) and PPARα in the fore-intestine. In the mid-intestine, dietary Zn reduced TAG content, activities of G6PD, ME, isocitrate dehydrogenase and FAS, down-regulated mRNA levels of 6PGD, G6PD, FAS, acetyl-CoA carboxylase a, PPARγ and SREBP-1, but up-regulated mRNA expression of HSLa, ATGL and PPARγ. The reduction in TAG content following Zn addition was attributable to reduced lipogenesis and increased lipolysis, and similar regulatory mechanisms were observed between the fore- and mid-intestine. [ABSTRACT FROM PUBLISHER]