scholarly journals 0868 Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 417-417
Author(s):  
L. Chen ◽  
B. A. Corl
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Binding Protein ◽  
Regulatory Element ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

scholarly journals β-Hydroxybutyrate Facilitates Fatty Acids Synthesis Mediated by Sterol Regulatory Element-Binding Protein1 in Bovine Mammary Epithelial Cells

2015 ◽  
Vol 37 (6) ◽  
pp. 2115-2124 ◽  
Author(s):  
Min Zhang ◽  
Shiqi Zhang ◽  
Qi Hui ◽  
Lin Lei ◽  
Xiliang Du ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Regulatory Element ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Control Group ◽  
Bovine Mammary Epithelial Cells ◽  
Sterol Regulatory Element

Background/Aims: In dairy cows, β-hydroxybutyrate (BHBA) is utilized as precursors of de novo synthesized fatty acids in mammary gland. Ketotic cows are characterized by excessive negative energy balance (NEB), which can further increase the blood BHBA concentration. Sterol regulatory element-binding protein1 (SREBP1) and cell death-inducing DNA fragmentation factor-alpha-like effector α (Cidea) play crucial roles in lipid synthesis. Therefore, we hypothesized that BHBA could stimulate SREBP1/Cidea pathway to increase milk fat synthesis in bovine mammary epithelial cells. Methods: Bovine mammary epithelial cells were treated with different concentrations of BHBA and transfected with adenovirus to silence SREBP1 expression. The effects of BHBA on the lipid synthesis in bovine mammary epithelial cells were investigated. Results: The results showed that BHBA could significantly increase the expression of SREBP1, fatty acid synthase (FAS), acetyl-CoA carboxylase α (ACC-α), Cidea and diacylglycerol transferase-1 (DGAT-1), as well as the triglycerides (TG) content in bovine mammary epithelial cells. BHBA treatment also increased the transfer of mature SREBP1 to nucleus compared with control group. However, SREBP1 silencing could significantly down-regulate the overexpression of FAS, ACC-α, Cidea and DGAT-1, as well as TG content induced by BHBA. Conclusion: The present data indicate that BHBA can significantly increase TG secretion mediated by SREBP1 in bovine mammary epithelial cells.

Transcriptional regulation of milk lipid synthesis by exogenous C16:0 and C18 fatty acids in bovine mammary epithelial cells

2018 ◽  
Vol 98 (2) ◽  
pp. 260-270 ◽  
Author(s):  
Ni Dan ◽  
Hang Zhang ◽  
Changjin Ao ◽  
Khas-Erdene
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Regulatory Element ◽  
Fatty Acid Synthetase ◽  
Mammary Epithelial ◽  
Lower Amount ◽  
Milk Lipid ◽  
Bovine Mammary Epithelial Cells

The objective of this study was to examine the effects of removing one fatty acid from a combination of long-chain fatty acids (LCFA) on milk lipogenesis in bovine mammary epithelial cells. The incubation concentration of LCFA was determined, and 100 μmol L−1 of C16:0, 5 μmol L−1 of C18:0, 100 μmol L−1 of cis-9 C18:1, 25 μmol L−1 of n-6 C18:2, and 1.2 μmol L−1 of n-3 C18:3 were used in the study. Treatments were C16:0, C18:0, C18:1, C18:2, and C18:3 combinations as control; control absent of C16:0 as A-C16:0; control absent of C18:0 as A-C18:0; control absent of C18:1 as A-C18:1; control absent of C18:2 as A-C18:2; control absent of C18:3 as A-C18:3. Results showed that compared with control, fatty acid synthetase expression was reduced by A-C18:0 and A-C18:1. Palmitic acid decreased expression of lipoprotein lipase. Compared with control, the expression of stearoyl-coenzyme A desaturase-1 and cluster of differentiation 36 was reduced by all treatments. Peroxisome proliferator-activated receptor-α expression was down-regulated by A-C16:0, A-C18:0, A-C18:1, and A-C18:2. Sterol regulatory element binding factor-1 was decreased when treated with A-C18:0, A-C18:1, and A-C18:2. Cells lack of 18-carbon fatty acid synthesized lower amount of intracellular triglyceride compared with control.

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