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首页> 外文期刊>Functional & integrative genomics >Sustained upregulation of stearoyl-CoA desaturase in bovine mammary tissue with contrasting changes in milk fat synthesis and lipogenic gene networks caused by lipid supplements
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Sustained upregulation of stearoyl-CoA desaturase in bovine mammary tissue with contrasting changes in milk fat synthesis and lipogenic gene networks caused by lipid supplements

机译:牛乳腺组织中硬脂酰辅酶A去饱和酶的持续上调,与脂质补充剂引起的乳脂合成和致脂基因网络变化形成鲜明对比

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摘要

Long-term mammary expression patterns of lipogenic gene networks due to dietary lipid remain largely unknown. Mammary tissue was biopsied for transcript profiling of 29 genes at 0, 7, and 21 days of feeding cows saturated lipid (EB100) or a blend of fish/soybean oil (FSO) to depress milk fat. Milk fat yield decreased gradually with FSO and coincided with lower molar yield of fatty acids synthesized de novo, stearic acid, and oleic acid. The PPARγ targets LPIN1 and SREBF1 along with ACSS2, ACACA, FASN, and LPL increased by day 7 of feeding EB100, but differences between diets disappeared by day 21. Expression of SCAP increased markedly over time with FSO and differed from EB100 by approximately sevenfold on day 21. Expression of THRSP decreased by day 7 with both diets and returned to basal levels by day 21. SCD expression increased linearly through 7 days and remained elevated with both diets, a likely mechanism to ensure the proper level of endogenous oleic acid via desaturation of dietary stearate (EB100) or via more SCD protein to account for the reduction in stearate supply from the rumen (FSO). Despite this response, endogenous oleate was insufficient to restore normal milk fat synthesis. Only 2 of 29 genes differed in expression between diets on day 21, suggesting that transcriptional control mechanisms regulating fat synthesis were established as early as 7 days post-feeding. Gene expression reflected vastly different physiological responses by mammary tissue to adjust its metabolism to the influx of saturated fatty acids, trans10-18:1, and/or to the lack of stearic acid.
机译:由于饮食脂质的致脂基因网络的长期乳腺表达模式仍然未知。在0、7和21天喂牛饱和脂质(EB100)或鱼/豆油(FSO)混合物压低乳脂后,对乳腺组织进行活检,以分析29个基因的转录谱。乳脂产量随着FSO逐渐降低,并且与从头合成的脂肪酸,硬脂酸和油酸的摩尔产量降低相吻合。 PPARγ靶向LPIN1和SREBF1以及ACSS2,ACACA,FASN和LPL在喂养EB100的第7天时增加,但饮食之间的差异在第21天消失。FCAP随时间的推移使SCAP的表达显着增加,并且与EB100的差异约为7倍。第21天,两种饮食在第7天时THRSP的表达均下降,而在第21天恢复到基础水平。两种饮食中SCD的表达均呈线性增加,并在两种饮食中均保持升高,这可能是通过去饱和来确保内源油酸水平适当的一种机制。饮食中的硬脂酸盐(EB100)或通过更多的SCD蛋白来解决瘤胃中硬脂酸盐供应的减少(FSO)。尽管有这种反应,内源性油酸盐不足以恢复正常的乳脂合成。在第21天的饮食之间,只有29个基因中的2个基因表达差异,这表明调节脂肪合成的转录控制机制最早在喂食后7天就建立了。基因表达反映了乳腺组织极大不同的生理反应,以调节其新陈代谢,使其适应饱和脂肪酸,trans10-18:1的流入和/或缺乏硬脂酸。

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