Regulation of the fatty acid synthase promoter by liver X receptor α through direct and indirect mechanisms in goat mammary epithelial cells

2015 ◽  
Vol 184 ◽  
pp. 44-51 ◽  
Author(s):  
Jun Li ◽  
Jun Luo ◽  
Jiangjiang Zhu ◽  
Yuting Sun ◽  
Dawei Yao ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Liver X Receptor ◽  
Mammary Epithelial ◽  
Liver X Receptor Α ◽  
Goat Mammary Epithelial Cells

Liver X receptor α participates in LPS-induced reduction of triglyceride synthesis in bovine mammary epithelial cells

2020 ◽  
pp. 1-7
Author(s):  
Jianfa Wang ◽  
Shuai Lian ◽  
Jun Song ◽  
Hai Wang ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Dairy Cow ◽  
Milk Fat ◽  
Mammary Epithelial Cells ◽  
Liver X Receptor ◽  
Mammary Epithelial ◽  
Triglyceride Synthesis ◽  
Milk Fat Depression ◽  
Liver X Receptor Α

Abstract Lipopolysaccharides (LPS) could induce milk fat depression via regulating the body and blood fat metabolism. However, it is not completely clear how LPS might regulate triglyceride synthesis in dairy cow mammary epithelial cells (DCMECs). DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS. The level of triglyceride synthesis, the expression and activity of the liver X receptor α (LXRα), enzymes related to de novo fatty acid synthesis, and the expression of the fatty acid transporters were investigated. We found that LPS decreased the level of triglyceride synthesis via a down-regulation of the transcription, translation, and nuclear translocation level of the LXRα. The results also indicated that the transcription level of the LXRα target genes, sterol regulatory element binding protein 1 (SREBP1), fatty acid synthetase (FAS), acetyl-CoA carboxylase-1 (ACC1), were significantly down-regulated in DCMECs after LPS treatment. Our data may provide new insight into the mechanisms of milk fat depression caused by LPS.

Inhibitions of FASN suppress triglyceride synthesis via the control of malonyl-CoA in goat mammary epithelial cells

2017 ◽  
Vol 57 (8) ◽  
pp. 1624 ◽  
Author(s):  
J. Luo ◽  
J. J. Zhu ◽  
Y. T. Sun ◽  
H. B. Shi ◽  
J. Li
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Fatty Acid Synthesis ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Acid Synthesis ◽  
Mammary Epithelial ◽  
Triglyceride Synthesis ◽  
Malonyl Coa ◽  
Goat Mammary Epithelial Cells

Fatty acid synthase (FASN) is the key enzyme for de novo fatty acid synthesis from acetyl-CoA and malonyl-CoA. All the steps involved in fatty acid synthesis by FASN have been clearly defined in monogastrics and ruminants. However, there are no data on the mechanism of how FASN affects triglyceride synthesis. Inhibition of FASN in goat mammary epithelial cells by C75, a synthetic inhibitor of FASN activity, and shRNA markedly suppressed the accumulation of triglyceride in goat mammary epithelial cells. Meanwhile, C75 treatment significantly reduced the relative content of monounsaturated fatty acids (C16:1 and C18:1). Corresponding to the suppression of lipid accumulation, both of C75 and shRNA also decreased the mRNA expression of GPAM, AGPAT6 and DGAT2, all of which are related to triglyceride synthesis. The fact that treatment of malonyl-CoA decreased the expression of these genes is consistent with the results of shRNA treatment. Furthermore, the supplement of malonyl-CoA enhanced the suppression on GPAM, AGPAT6, LPIN1, DGAT1 and DGAT2. The results underscore the role of malonyl-CoA in inhibition of FASN in regulating triglyceride synthesis in goat mammary epithelial cells.

scholarly journals GosB Inhibits Triacylglycerol Synthesis and Promotes Cell Survival in Mouse Mammary Epithelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Gaoxiao Xu ◽  
Saixing Duan ◽  
Jianye Hou ◽  
Zhongxin Wei ◽  
Guangwei Zhao
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Milk Fat ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Milk Fatty Acid ◽  
Fatty Acid Binding ◽  
Triacylglycerol Synthesis

It has been demonstrated that the activator protein related transcription factor Finkel-Biskis-Jinkins murine osteosarcoma B (GosB) is involved in preadipocyte differentiation and triacylglycerol synthesis. However, the role of GosB in regulating the synthesis of milk fatty acid in mouse mammary glands remains unclear. This research uncovered potentially new roles of GosB in suppressing milk fatty acid synthesis. Results revealed that GosB had the highest expression in lung tissue and showed a higher expression level during nonlactation than during lactation. GosB inhibited the expression of fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), fatty acid binding protein 4 (FABP4), diacylglycerol acyltransferase 1 (DGAT1), perilipin 2 (PLIN2), perilipin 3 (PLIN3), and C/EBPα in mouse mammary gland epithelial cells (MEC). In addition, GosB reduced cellular triglyceride content and the accumulation of lipid droplets; in particular, GosB enhanced saturated fatty acid concentration (C16:0 and C18:0). The PPARγ agonist, rosiglitazone (ROSI), promoted apoptosis and inhibited cell proliferation. GosB increased the expression of Bcl-2 and protected MEC from ROSI-induced apoptosis. Furthermore, MECs were protected from apoptosis through the GosB regulation of intracellular calcium concentrations. These findings suggest that GosB may regulate mammary epithelial cells milk fat synthesis and apoptosis via PPARγ in mouse mammary glands.

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