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Excessive fat deposition in the hepatocytes, associated with excess dietary fat intake, was related to the occurrence of fatty livers in fish. miR-101b plays the important roles in controlling lipid metabolism, but the underlying mechanism at the post-transcriptional level remains unclear. The purpose of this study is to explore the roles and mechanism of miR-101b-mediating lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco . We found that miR-101b directly targeted fatty acid translocase ( cd36 ), caspase9 ( casp9 ) and autophagy-related gene 4A ( atg4a ). Furthermore, using palmitic acid (PA) or oleic acid (OA) to incubate the primary hepatocytes of yellow catfish, we demonstrated that miR-101b inversely regulated cd36 , casp9, and atg4a expression at the transcriptional level; the inhibition of miR-101b aggravated fatty acids (FAs, PA or OA)-induced lipid accumulation, indicating that miR-101b mediated FAs-induced variations of lipid metabolism in yellow catfish. Taken together, our study gave novel insight into the regulatory mechanism of lipid deposition and metabolism and might provide potential targets for the prevention and treatment of fatty livers in fish.

The activating transcription factor 4 (ATF4), DNA damage-inducible transcript 3 (DDIT3), growth arrest, and DNA damage-inducible protein 34 (GADD34), endoplasmic reticulum oxidoreductin 1α (ERO1α), and tumor necrosis factor receptor associated factor 2 (TRAF2) cDNAs were first characterized from yellow catfish Pelteobagrus fulvidraco. Compared to corresponding genes of mammals, all of these proteins shared similar conserved domains. Their mRNAs were widely expressed in various tissues, but at variable levels. Dietary lipid levels did not significantly influence ATF4 mRNA expression. mRNA expression of DDIT3 and GADD34 was highest for fish fed the low-lipid diets and lowest for fish fed middle-lipid diets. The mRNA levels of ERO1α and TRAF2 declined with increasing dietary lipid levels. For the first time, we characterized the full-length cDNA sequences of ATF4, DDIT3, GADD34, ERO1α, and TRAF2 and determined their tissue expression profiles and transcriptional responses to dietary lipid levels, which would contribute to our exploration into their biological functions, and providing new insights on relations between ER stress and lipid metabolism in fish.

The present working hypothesis is that the Cu-induced changes in lipid metabolism may be mediated by miRNAs. Here, we describe the miRNA profile of the liver tissues of yellow catfish exposed to waterborne Cu, based on larger-scale sequencing of small RNA libraries. We identified a total of 172 distinct miRNAs. Among these miRNAs, compared to the control, mRNA expression levels of 16 miRNAs (miR-203a, 205, 1788-3p, 375, 31, 196a, 203b-3p, 2187-5p, 196d, 459-3p, 153a and miR-725, and two novel-miRNAs: chr4-1432, chr-7684) were down-regulated, and mRNA levels of miR-212 and chr20-5274 were up-regulated in Cu-exposed group. The functions of their target genes mainly involved ether lipid metabolism, glycerophospholipid metabolism, linoleic acid metabolism and α-linolenic acid metabolism. Cu exposure inhibited the expression of miR-205, whose predicted target genes were enriched in the pathway of lipid metabolism, including fas , lxrα , ddit3 , lamp2 , casp3a and baxa . These potential target genes were further verified by Dual-luciferase reporter gene assay. Using primary hepatocytes of yellow catfish, Cu incubation down-regulated miR-205 expression, and increased TG contents and FAS activity. LXR antagonist effectively ameliorate the Cu-induced change of TG content and FAS activity. These data suggest that down-regulation of the miRNA-205 may be an important step in Cu-induced changes in lipid metabolism in yellow catfish.

The present study explored the influence of Zn addition in the water on Zn transport and lipid metabolism of two intestinal regions in goby Synechogobius hasta. Zn contents in water were 0.004 (control), 0.181 and 0.361mg Zn L -1 , respectively. The experiment lasted for 28 days. TG and Zn contents, mRNA contents of genes of Zn transport and lipid metabolism, and enzyme activity from anterior and mid-intestine tissues were analyzed. In anterior intestine, Zn addition in the water increased Zn contents, and mRNA concentrations of ZIP4, ZIP5, ATGL, PPARα, ZNF202 and KLF7, decreased TG contents, 6PGD and G6PD activities, and mRNA contents of 6PGD, G6PD, FAS, PPARγ, ICDH and KLF4. In mid-intestine tissue, the highest Zn and TG contents were observed for 0.18mg Zn/l group, in parallel with the highest expressions of ZnT1, ZIP4, ZIP5, 6PGD, FAS, ICDH, PPARγ, PPARα, ZNF202, KLF4 and KLF7, and with the highest FAS, 6PGD and G6PD activities. Thus, in the anterior intestine, Zn addition increased lipolysis and decreased lipogenesis, and accordingly reduced TG content. However, the highest mid-intestinal TG content in 0.18mg Zn/l group was due to the up-regulated lipogenesis. Although lipolysis was also increased, the incremental lipid synthesis was enough to compensate for lipid degradation, which led TG accumulation. Our results, for the first time, show an anterior/mid functional regionalization of the intestine in lipid metabolism and Zn transport of S. hasta following Zn exposure., (Copyright © 2017 Elsevier Inc. All rights reserved.)

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.

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]

Currently, the effect of selenium and oxidized fish oil interactions on the intestinal lipid metabolism and antioxidant responses of fish remains unknown. Herein, yellow catfish Pelteobagrus fulvidraco (weight: 3.99 ± 0.01 g) were used as experimental animals and were fed four diets: an adequate amount of selenium (0.25 mg kg−1) with fresh fish oil (A-Se+FFO), an adequate amount of selenium with oxidized fish oil (A-Se+OFO), a high amount of selenium (0.50 mg kg−1) with fresh fish oil (H-Se+FFO), and a high amount of selenium with oxidized fish oil (H-Se+OFO). The feeding experiment was conducted for 10 weeks. The results showed that selenium supplementation alleviated the intestinal tissue damage and reduced the lipid accumulation that was induced by oxidized fish oils. Meanwhile, we also found that 0.50 mg kg−1 selenium reduced the oxidative stress that is caused by oxidized fish oils through increasing the GSH and the activity and mRNA expression of antioxidant enzymes. Dietary selenium and oxidized fish oils also affected the mRNA expression of intestinal selenoproteins including selenow2a, selenop2, and selenot2. Mechanistically, Se and oxidized eicosapentaenoic acid (oxEPA) influenced the GSH content by affecting the DNA binding ability of activating transcription factor (ATF) 3 to the slc7a11 promoter. For the first time, our results suggested that selenium alleviated the oxidized fish oil-induced intestinal lipid deposition and the oxidative stress of the fish. We also elucidated the novel mechanism of selenium increasing the GSH content by affecting the interaction of ATF3 and the slc7a11 promoter. [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]

Background: The intestine is the main organ for absorbing dietary fat. High dietary lipid intake leads to fat deposition in the intestine and adversely influences fat absorption and health, but the underlying mechanism is unknown.Objectives: We used yellow catfish and their isolated intestinal epithelial cells to test the hypothesis that endoplasmic reticulum (ER) stress, autophagy, and apoptosis mediate fat-induced changes in lipid metabolism.Methods: Male and female yellow catfish (weight: 3.79 ± 0.16 g; age: 3 mo) were fed diets containing lipid at 6.98% (low-fat diet; LFD), 11.3% (middle-fat diet; MFD), or 15.4% (high-fat diet; HFD) (by weight) for 8 wk. Each dietary group had 3 replicates, 30 fish per replicate. Their intestinal epithelial cells were isolated and incubated for 24 h in control solution or various concentrations of fatty acids (FAs) with or without 2-h pretreatment with an inhibitor [3-methyladenine (3-MA), 4-phenyl butyric acid (4-PBA), or Ac-DVED-CHO (AC)]. Triglyceride (TG) contents, genes, and enzymes involved in lipid metabolism, ER stress, autophagy, and apoptosis were determined in intestinal tissue and cells; immunoblotting, BODIPY 493/503 staining, ultrastructural observation, and the detection of autophagic and apoptotic vesicles were performed on intestinal cells.Results: Compared with the LFD and MFD, the HFD increased intestinal TG content by 120-226%, activities of lipogenic enzymes by 19.0-245%, expression of genes related to lipogenesis (0.77-8.4-fold), lipolysis (0.36-6.0-fold), FA transport proteins (0.79-1.7-fold), ER stress (0.55-7.5-fold), autophagy (0.56-4.2-fold), and apoptosis (0.80-5.2-fold). Using isolated intestinal epithelial cells and inhibitors (4-PBA, 3-MA, and AC), we found that ER stress mediated FA-induced activation of autophagy (11.0-50.1%) and apoptosis (10.4-32.0%), and lipophagy and apoptosis mediated FA-induced lipolysis (3.40-41.6%).Conclusions: An HFD upregulated lipogenesis, lipolysis, and FA transport, induced ER stress, and activated autophagy and apoptosis. ER stress, autophagy, and apoptosis play important regulatory roles in fat-induced changes in lipid metabolism in the intestine and intestinal epithelial cells of yellow catfish. [ABSTRACT FROM AUTHOR]

Mounting evidence showed that excess selenium (10.0–15.0-fold of adequate Se) intake caused severe hepatic lipid deposition in the vertebrate. However, the underlying mechanism remains unclear. The study was performed to elucidate the mechanism of Se supranutrition mediated-changes of lipid deposition and metabolism. We found that dietary excessive Se addition increased hepatic TGs and glucose contents, up-regulated lipogenic enzyme activities and reduced hepatic glycogen contents. Transcriptomic and immunoblotting analysis showed that Se supranutrition significantly influenced serine/threonine kinase 1 (AKT1)-forkhead box O3a (FOXO3a)-PYGL signaling and protein levels of SELENOF. Knockdown of SELENOF and PYGL by RNA interference revealed that the AKT1-FOXO3a-PYGL axis was critical for Se supranutrition-induced lipid accumulation. Moreover, Se supranutrition-induced lipid accumulation was via the increased DNA binding capacity of FOXO3a to PYGL promoter, which increased glycogenolysis, and accordingly promoted lipogenesis and lipid accumulation. Our finding provides new insight into the mechanism of Se supranutrition-induced lipid accumulation and suggests that SELENOF may be a therapeutic target for Se supranutrition induced-lipid disorders in the vertebrates. [Display omitted] • Excessive Se intake increased induced lipid deposition and decreased glycogen content; • Se decreased phosphorylation of AKT1 and affected FOXO3a nuclear translocation; • SELENOF mediated Se-induced changes of TGs and glycogen contents; • AKT1-FOXO3a-PYGL pathway mediated these physiological processes.. [ABSTRACT FROM AUTHOR]

At present, studies involved in the effects of dietary Se sources on lipid metabolism were very scarce and the underlying mechanism remains unknown. Previous studies reported that dietary Se sources differentially affected selenoprotein S (SELENOS) expression and SELENOS affected lipid metabolism via the inositol-requiring enzyme 1α (IRE1α)- spliced X-box binding protein 1 (XBP1s) pathway. Thus, we used yellow catfish as an experimental model to explore whether dietary selenium sources affected the hepatic lipid metabolism, and further determined the role of SELENOS-IRE1α-XBP1s pathway in dietary selenium sources affecting hepatic lipid metabolism. Compared with the selenomethionine (S-M) group, sodium selenite (S S) group possessed higher liver triglycerides (TGs) (34.7%), lipogenic enzyme activities (57.9–70.6%), and lower antioxidant enzyme activities (23.3–35.5%), increased protein levels of heat shock transcription factor 1 (HSF1) and SELENOS (1.17-fold and 47.4%, respectively), and XBP1s- peroxisome proliferators-activated receptor γ (PPARγ) pathway. Blocking SELENOS and PPARγ by RNA interference demonstrated that the SELENOS/XBP1s/PPARγ axis was critical for S-S-induced lipid accumulation. Moreover, S-S-induced upregulation of SELENOS was via the increased DNA binding capacity of HSF1 to SELENOS promoter, which activated the XBP1s/PPARγ pathway and promoted lipogenesis and lipid accumulation. XBP1s is required for S-S-induced upregulation of PPARγ expression. Our finding elucidated the mechanism of dietary Se sources affecting the lipid metabolism in the liver of yellow catfish and demonstrated novel function of SELENOS in metabolic regulation. Our study also suggested that seleno-methionine was a better Se source than selenite against abnormal lipid deposition in the liver of yellow catfish. [Display omitted] • Dietary inorganic Se increased TGs content and up-regulated lipogenesis. • Dietary inorganic Se increased protein levels of HSF1 and SELENOS. • SELENOS/XBP1s/PPARγ axis was critical for inorganic Se-induced TG deposition. • Inorganic Se induced SELENOS expression via the increased HSF1 binding to its promoter. • XBP1s is required for inorganic Se-induced upregulation of PPARγ expression and lipogenesis. [ABSTRACT FROM AUTHOR]

• Oxidized fish oil increased lipid content by ROS-induced mitochondria dysfunction. • OxEPA-activated lipophagy was via inhibiting the CREB-1-Bcl-2-Beclin1 pathway. • Our study demonstrated the mechanisms of oxidized fish oils increasing lipid deposition. • Fish oils supplements after oxidization is harmful for obese and NAFLD patients. At present, the harmful effects and relevant mechanism of oxidized fish oils on fish and fish cells remain unknown. Our study found that oxidized fish oils increased lipogenesis, and reduced lipolysis, activated oxidative stress by decreasing glutathione peroxidase (GPX) activity, increasing malondialdhyde (MDA) content and damaging mitochondrial structure, and activated autophagy in the liver of yellow catfish; oxidized eicosapentaenoic acid (oxEPA) induced oxidative stress in yellow catfish hepatocytes. Oxidative stress, mitochondrial dysfunction and lipophagy mediated oxEPA induced-variations in lipid metabolism. Our further investigation indicated that oxEPA-activated lipophagy was via inhibiting the DNA binding capacity of the cAMP-response element binding protein (CREB)-1 to the region of Bcl-2 promoter, which in turn suppressed the binding activity of Bcl-2 to Beclin1 and promoted autophagosome formation. For the first time, our study elucidated the mechanisms of oxidized fish oils-induced lipid deposition by the oxidative stress, mitochondrial dysfunction and CREB1-Bcl-2-Beclin1 pathway in fish. [ABSTRACT FROM AUTHOR]

Selenium (Se) is an essential micro-mineral and plays important roles in antioxidant responses, and also influences lipid metabolism and selenoprotein expression in vertebrates, but the effects and mechanism remain unknown. The study was undertaken to decipher the insights into dietary Se influencing lipid metabolism and selenoprotein expression in the anterior and middle intestine (AI and MI) of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (weight: 8.27 ± 0.03 g) were fed a 0.03- (M-Se), 0.25- (A-Se), or 6.39- (E-Se) mg Se/kg diet for 12 wk. AI and MI were analyzed for triglycerides (TGs) and Se concentrations, histochemistry and immunofluorescence, enzyme activities, and gene and protein levelsassociated with antioxidant responses, lipid metabolism, endoplasmic reticulum (ER) stress, and selenoproteome. Compared to the A-Se group, M-Se and E-Se diets significantly decreased weight gain (WG) and increased TGs concentration in the AI and MI. In the AI, compared with A-Se group, M-Se and E-Se diets significantly increased activities of fatty acid synthase, expression of lipogenic genes, and suppressed lipolysis. In the MI, compared to the A-Se group, M-Se and E-Se diets significantly increased activities of lipogenesis and expression of lipogenic genes. Compared with A-Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the AI and MI, and M-Se diet did not significantly reduce GPX activities in the AI and MI. Compared with the A- Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the plasma and liver, and M-Se diet significantly reduced GPX activities in the plasma and liver. Compared with the A-Se group, M-Se and E-Se groups also increased glucose-regulated protein 78 (GRP78, ER stress marker) protein expression of the intestine. Dietary Se supplementation also differentially influenced the expression of the 28 selenoproteins in the AI and MI, many of which possessed antioxidant characteristics. Compared with the A-Se group, the M-Se group significantly decreased mRNA levels of txnrd2 and txnrd3, but made no difference on mRNA levels of these seven GPX proteins in the MI. Moreover, we characterized sterol regulatory element binding protein 1c (SREBP1c) binding sites of three ER-resident proteins (selenom, selenon, and selenos) promoters, and found that Se positively controlled selenom, selenon, and selenos expression via SREBP1c binding to the selenom, selenon, and selenos promoter. Thus, dietary marginal and excess Se increased TGs deposition of yellow catfish P. fulvidraco, which might be mediated by ER-resident selenoproteins expression and ER stress. [ABSTRACT FROM AUTHOR]

The present study was conducted to explore the mechanism of nano-Zn absorption and its influence on lipid metabolism in the intestine of yellow catfish Pelteobagrus fulvidraco. Compared to ZnSO4, dietary nano-Zn addition increased the triglyceride (TG) content, enzymatic activities of malic enzyme (ME) and fatty acid synthase (FAS), and up-regulated mRNA levels of 6pgd, fas, acca, dgat1, pparγ, and fatp4. Using primary intestinal epithelial cells of yellow catfish, compared to the ZnSO4 group, nano-Zn incubation increased the contents of TG and free fatty acids (FFA), the activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6GPD), ME, and FAS, up-regulated mRNA levels of lipogenic genes (6pgd, g6pd, fas, dgat1, and pparγ), genes of lipid transport (fatp4 and ifabp), and Zn transport genes (znt5, znt7, mt, and mtf1), and increased the protein expression of fatty acid transport protein 4 (FATP4) and peroxisome proliferator activated receptor gamma (PPARγ). Further studies found that nano-Zn absorption was via the clathrin-dependent endocytic mechanism. PPARγ mediated the nano-Zn-induced increase in TG, and nano-Zn increased Zn accumulation and induced TG accumulation by activating the PPARγ pathway and up-regulating lipogenesis. [ABSTRACT FROM AUTHOR]

Aims: Excessive manganese (Mn) exposure is toxic, and induces lipid deposition, but the underlying mechanisms remain elusive. Herein, we explored how dietary Mn supplementation affects lipid deposition and metabolism in the intestine of vertebrates using the yellow catfish Pelteobagrus fulvidraco as the model. Results: High-Mn (H-Mn) diet increased intestinal Mn content, promoted lipid accumulation and lipogenesis, and inhibited lipolysis. In addition, it induced oxidative stress, upregulated metal-response element-binding transcription factor-1 (MTF-1), and peroxisome proliferator-activated receptor gamma (PPARγ) protein expression in the nucleus, induced PPARγ acetylation, and the interaction between PPARγ and retinoid X receptor alpha (RXRα), while it downregulated sirtuin 1 (SIRT1) expression and activity. Mechanistically, Mn activated the MTF-1/divalent metal transporter 1 (DMT1) pathway, increased Mn accumulation in the mitochondria, and induced oxidative stress. This in turn promoted lipid deposition via deacetylation of PPARγ at K339 by SIRT1. Subsequently, PPARγ mediated Mn-induced lipid accumulation through transcriptionally activating fatty acid translocase, stearoyl-CoA desaturase 1, and perilipin 2 promoters. Innovation: These studies uncover a previously unknown mechanism by which Mn induces lipid deposition in the intestine via the oxidative stress–SIRT1–PPARγ pathway. Conclusion: High dietary Mn intake activates MTF-1/DMT1 and oxidative stress pathways. Oxidative stress-mediated PPARγ deacetylation at K339 site contributes to increased lipid accumulation. Our results provided a direct link between Mn and lipid metabolism via the oxidative stress–SIRT1–PPARγ axis. Antioxid. Redox Signal. 37, 417–436. [ABSTRACT FROM AUTHOR]

The present study was conducted to evaluate the influences of five dietary manganese (Mn) sources on growth, feed utilization, lipid metabolism, antioxidant capacity, inflammatory response and endoplasmic reticulum stress in intestinal tissues of yellow catfish Pelteobagrus fulvidraco. Five Mn sources include Mn sulfate monohydrate (MnSO 4 ·H 2 O), Mn dioxide (MnO 2), Mn dioxide nanoparticles (MnO 2 NPs), Mn glycine chelate (Mn-Gly) and hydroxymethionine-chelated Mn (Mn-MHA). Yellow catfish (initial body weight: 2.69 ± 0.01 g/fish) were fed five experimental diets for 10 weeks. Dietary Mn sources significantly affected intestinal Mn content and metabolism. Compared to other Mn sources, yellow catfish fed organic Mn sources (Mn-Gly and Mn-MHA) tended to improve growth, feed utilization, intestinal histology, up-regulated mRNA abundance of tight junction-relevant genes, increased intestinal fatty acid uptake and transport and triglyceride deposition, and reduced inflammatory responses. These dietary organic Mn supplements also increased intestinal antioxidant capacity by up-regulating antioxidant gene expression and enzymatic activities. Yellow catfish fed two organic Mn diets had the lower mRNA expressions of endoplasmic reticulum stress-relevant gene and protein expression. Based on these observations above, dietary organic supplements (Mn-Gly and Mn-MHA) improved the growth and feed utilization, and promoted intestinal health of yellow catfish, and accordingly seems to be optimal Mn sources for yellow catfish. Our results provided the innovative insights into dietary Mn sources influencing tight junction, antioxidant capacity and inflammatory responses, endoplasmic reticulum stress and fatty acid uptake and uptake in the fish intestine, and found that organic Mn sources were more suitable as the Mn supplements in yellow catfish feeds, and also possibly in other aquatic feed. • Two organic Mn sources in yellow catfish diet positively affect growth performance. • Two organic Mn sources in yellow catfish diet improved intestinal tight junction. • Two organic Mn in yellow catfish diet increased fatty acid uptake and TG deposition. • Two organic Mn reduced intestinal inflammation and increased antioxidant capacity. • Two organic Mn sources in yellow catfish diet improved the ER function. [ABSTRACT FROM AUTHOR]