首页> 外文期刊>Canadian Journal of Animal Science >Transcriptional regulation of milk lipid synthesis by exogenous C16:0 and C18 fatty acids in bovine mammary epithelial cells
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Transcriptional regulation of milk lipid synthesis by exogenous C16:0 and C18 fatty acids in bovine mammary epithelial cells

机译:外源C16:0和C18牛乳腺上皮细胞中C16脂肪酸的转录调节

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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 mu mol L-1 of C16:0, 5 mu mol L-1 of C18:0, 100 mu mol L-1 of cis-9 C18:1, 25 mu mol L-1 of n-6 C18:2, and 1.2 mu mol 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-a expression was downregulated 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.
机译:本研究的目的是研究从牛乳腺上皮细胞中牛奶脂肪生成的长链脂肪酸(LCFA)组合中除去一种脂肪酸的作用。测定LCFA的孵育浓度,C16:0,5μmol1-1的100μmolL-1,C18:0,100mol L-1的C18:0,100mol L-1,25μm10,在研究中使用N-6 C18:2的N-6 C18:2和1.2μmolL-1中的1.2μmolL-1。治疗为C16:0,C18:0,C18:1,C18:2和C18:3组合作为对照;控制不存在C16:0作为A-C16:0;控制不存在C18:0作为A-C18:0;控制不存在C18:1作为A-C18:1;控制不存在C18:2作为A-C18:2;控制不存在C18:3作为A-C18:3。结果表明,与对照相比,A-C18:0和A-C18:1减少了脂肪酸合成酶表达。棕榈酸降低脂蛋白脂肪酶的表达。与对照相比,所有治疗都减少了硬脂酰基辅酶的表达和分化36的表达。通过A-C16:0,A-C18:0,A-C18:1和A-C18:2下调过氧化物体增殖物激活的受体-A表达。当用A-C18:0,A-C18:1和A-C18:2处理时,甾醇调节元件结合因子-1减少。与对照相比,细胞缺乏18-碳脂肪酸合成细胞内甘油三酯。

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