Identification of five genes in endoplasmic reticulum (ER) stress–apoptosis pathways in yellow catfish Pelteobagrus fulvidraco and their transcriptional responses to dietary lipid levels

2019 ◽  
Vol 45 (3) ◽  
pp. 1117-1127
Author(s):  
Dian-Guang Zhang ◽  
Jie Cheng ◽  
Zhi-Peng Tai ◽  
Zhi Luo
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Dietary Lipid ◽  
Pelteobagrus Fulvidraco ◽  
Lipid Levels ◽  
Yellow Catfish ◽  
Transcriptional Responses ◽  
Apoptosis Pathways

scholarly journals Dietary lipid levels requirements of hybrid yellow catfish (Pelteobagrus fulvidraco × P. vachelli

2021 ◽  
Author(s):  
Gobeng L.S. Mamuru ◽  
Jun Qiang ◽  
Yi-Fan Tao ◽  
De-Ju Chen ◽  
Jing-Wen Bao ◽  
...  
Keyword(s):  
Dietary Lipid ◽  
Pelteobagrus Fulvidraco ◽  
Lipid Levels ◽  
Yellow Catfish

scholarly journals Dietary Marginal and Excess Selenium Increased Triglycerides Deposition, Induced Endoplasmic Reticulum Stress and Differentially Influenced Selenoproteins Expression in the Anterior and Middle Intestines of Yellow Catfish Pelteobagrus fulvidraco

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 535
Author(s):  
Dian-Guang Zhang ◽  
Tao Zhao ◽  
Xiao-Jian Xu ◽  
Wu-Hong Lv ◽  
Zhi Luo
Keyword(s):  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Glutathione Peroxidase ◽  
Er Stress ◽  
Fatty Acid Synthase ◽  
Pelteobagrus Fulvidraco ◽  
Mrna Levels ◽  
Yellow Catfish ◽  
Antioxidant Responses ◽  
Lipogenic Genes

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.

scholarly journals Effects of Fat and Fatty Acids on the Formation of Autolysosomes in the Livers from Yellow Catfish Pelteobagrus Fulvidraco

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 751 ◽  
Author(s):  
Wu ◽  
Wei ◽  
Yang ◽  
Zhao ◽  
Luo
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Pelteobagrus Fulvidraco ◽  
Mrna Levels ◽  
High Fat ◽  
Primary Hepatocytes ◽  
Yellow Catfish ◽  
Transcriptional Responses

The autophagy-lysosome pathway, which involves many crucial genes and proteins, plays crucial roles in the maintenance of intracellular homeostasis by the degradation of damaged components. At present, some of these genes and proteins have been identified but their specific functions are largely unknown. This study was performed to clone and characterize the full-length cDNA sequences of nine key autolysosome-related genes (vps11, vps16, vps18, vps33b, vps41, lamp1, mcoln1, ctsd1 and tfeb) from yellow catfish Pelteobagrus fulvidraco. The expression of these genes and the transcriptional responses to a high-fat diet and fatty acids (FAs) (palmitic acid (PA) and oleic acid (OA)) were investigated. The mRNAs of these genes could be detected in heart, liver, muscle, spleen, brain, mesenteric adipose tissue, intestine, kidney and ovary, but varied with the tissues. In the liver, the mRNA levels of the nine autolysosome-related genes were lower in fish fed a high-fat diet than those fed the control, indicating that a high-fat diet inhibited formation of autolysosomes. Palmitic acid (a saturated FA) significantly inhibited the formation of autolysosomes at 12 h, 24 h and 48 h incubation. In contrast, oleic acid (an unsaturated FA) significantly induced the formation of autolysosomes at 12 h, but inhibited them at 24 h. At 48 h, the effects of OA incubation on autolysosomes were OA concentration-dependent in primary hepatocytes of P. fulvidraco. The results of flow cytometry and laser confocal observations confirmed these results. PA and OA incubation also increased intracellular non-esterified fatty acid (NEFA) concentration at 12 h, 24 h and 48 h, and influenced mRNA levels of fatty acid binding protein (fabp) and fatty acid transport protein 4 (fatp4) which facilitate FA transport in primary hepatocytes of P. fulvidraco. The present study demonstrated the molecular characterization of the nine autolysosome-related genes and their transcriptional responses to fat and FAs in fish, which provides the basis for further exploring their regulatory mechanism in vertebrates.

scholarly journals Endoplasmic Reticulum Stress–Mediated Autophagy and Apoptosis Alleviate Dietary Fat–Induced Triglyceride Accumulation in the Intestine and in Isolated Intestinal Epithelial Cells of Yellow Catfish

2019 ◽  
Vol 149 (10) ◽  
pp. 1732-1741 ◽  
Author(s):  
Shi-Cheng Ling ◽  
Kun Wu ◽  
Dian-Guang Zhang ◽  
Zhi Luo
Keyword(s):  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Er Stress ◽  
Dietary Fat ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Yellow Catfish ◽  
Triglyceride Accumulation ◽  
Induced Changes

ABSTRACTBackgroundThe 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.ObjectivesWe 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.MethodsMale 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.ResultsCompared 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%).ConclusionsAn 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.

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