Effects of insulin and its related signaling pathways on lipid metabolism in the yellow catfish Pelteobagrus fulvidraco

2015 ◽  
Vol 218 (19) ◽  
pp. 3083-3090 ◽  
Author(s):  
M.-Q. Zhuo ◽  
Z. Luo ◽  
Y.-X. Pan ◽  
K. Wu ◽  
Y.-F. Fan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Signaling Pathways ◽  
Pelteobagrus Fulvidraco ◽  
Yellow Catfish

scholarly journals miR-101b Regulates Lipid Deposition and Metabolism of Primary Hepatocytes in Teleost Yellow Catfish Pelteobagrus fulvidraco

Genes ◽  
2020 ◽  
Vol 11 (8) ◽  
pp. 861
Author(s):  
Guang-Hui Chen ◽  
Tao Zhao ◽  
Xiao-Lei Wei ◽  
Dian-Guang Zhang ◽  
Mei-Qin Zhuo ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Underlying Mechanism ◽  
Pelteobagrus Fulvidraco ◽  
Transcriptional Level ◽  
Lipid Deposition ◽  
Fat Intake ◽  
Primary Hepatocytes ◽  
Yellow Catfish ◽  
Fatty Livers ◽  
Insight Into

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.

scholarly journals Dietary Nano-ZnO Is Absorbed via Endocytosis and ZIP Pathways, Upregulates Lipogenesis, and Induces Lipotoxicity in the Intestine of Yellow Catfish

2021 ◽  
Vol 22 (21) ◽  
pp. 12047
Author(s):  
Shu-Wei Chen ◽  
Wu-Hong Lv ◽  
Kun Wu ◽  
Guang-Hui Chen ◽  
Fang Chen ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Farnesoid X Receptor ◽  
Pelteobagrus Fulvidraco ◽  
Yellow Catfish ◽  
Nano Zno ◽  
Expression Levels ◽  
Mrna Expression Levels

Nano-sized zinc oxide (nano-ZnO) affects lipid deposition, but its absorption patterns and mechanisms affecting lipid metabolism are still unclear. This study was undertaken to investigate the molecular mechanism of nano-ZnO absorption and its effects on lipid metabolism in the intestinal tissues of a widely distributed freshwater teleost yellow catfish Pelteobagrus fulvidraco. We found that 100 mg/kg dietary nano-ZnO (H-Zn group) significantly increased intestinal Zn contents. The zip6 and zip10 mRNA expression levels were higher in the H-Zn group than those in the control (0 mg/kg nano-ZnO), and zip4 mRNA abundances were higher in the control than those in the L-Zn (50 mg/kg nano-ZnO) and H-Zn groups. Eps15, dynamin1, dynamin2, caveolin1, and caveolin2 mRNA expression levels tended to reduce with dietary nano-ZnO addition. Dietary nano-ZnO increased triglyceride (TG) content and the activities of the lipogenic enzymes glucose 6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), and isocitrate dehydrogenase (ICDH), upregulated the mRNA abundances of lipogenic genes 6pgd, fatty acid synthase (fas), and sterol regulatory element binding protein 1 (srebp1), and reduced the mRNA expression of farnesoid X receptor (fxr) and small heterodimer partner (shp). The SHP protein level in the H-Zn group was lower than that in the control and the L-Zn group markedly. Our in vitro study indicated that the intestinal epithelial cells (IECs) absorbed nano-ZnO via endocytosis, and nano-Zn-induced TG deposition and lipogenesis were partially attributable to the endocytosis of nano-ZnO in IECs. Mechanistically, nano-ZnO-induced TG deposition was closely related to the metal responsive transcription factor 1 (MTF-1)-SHP pathway. Thus, for the first time, we found that the lipogenesis effects of nano-ZnO probably depended on the key gene shp, which is potentially regulated by MTF1 and/or FXR. This novel signaling pathway of MTF-1 through SHP may be relevant to explain the toxic effects and lipotoxicity ascribed to dietary nano-ZnO addition.

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