Abstract

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.

Highlights

  • Selenium (Se) is an essential trace element and plays important roles in antioxidant responses among vertebrates

  • E-Se diets significantly decreased weight gain (WG) compared with A-Se group (Table 1)

  • Se enhanced the binding activity of sterol regulatory element binding protein 1c (SREBP1c) (Figures 8F, 9D and 10D), suggesting that the −435/−426 bp region of selenos promoter, −175/−166 bp region of selenom promoter and −1330/−1321 bp region of selenon promoter were functional binding sites for SREBP1c binding. These findings indicated that SREBP1c mediated the transcriptional response of selenos, selenom, and selenon to Se

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Summary

Introduction

Selenium (Se) is an essential trace element and plays important roles in antioxidant responses among vertebrates. Studies suggested that dietary Se addition influenced lipid deposition and metabolism [3,4,5]. Studies reported that the collective responses of selenotranscriptome varied with dietary Se contents and the tissues [3,4,7,8,9]. Among all these studies mentioned above, the intestine tissues are absent in their analysis. Highlighting the important role of the intestine regionalization in nutrient uptake and metabolism, it is worth exploring the response of selenotranscriptomes and lipid metabolism in two intestinal regions, such as anterior intestine (AI) and middle intestine (MI), to dietary Se addition

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