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首页> 外文会议>Cornell Nutrition Conference for Feed Manufacturers >DEVELOPING PRACTICAL APPROACHES TO MODIFY HEPATIC FATTY ACID PROCESSING AND LIPID MEDIATOR BIOSYNTHESIS IN DAIRY CATTLE: THE EMERGING ROLE OF LIPIDOMICS
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DEVELOPING PRACTICAL APPROACHES TO MODIFY HEPATIC FATTY ACID PROCESSING AND LIPID MEDIATOR BIOSYNTHESIS IN DAIRY CATTLE: THE EMERGING ROLE OF LIPIDOMICS

机译：制定切换肝脏脂肪酸加工和脂质介质生物合成的实用方法：脂类物学的新兴作用

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Postpartum metabolic disease in dairy cattle involves the development of adipose tissue insulin resistance and hepatic lipid accretion. Although the adverse interplay between these metabolic organs is accepted, the cellular mechanisms that contributeto impaired insulin action and steatosis are not completely understood. Indeed, early lactation insulin resistance promotes adipose tissue lipolysis and dyslipidemia increases the hepatic uptake of fatty acids (FA). As a consequence, steatosis develops because of inadequate mitochondrial p-oxidation, enhanced triacylglycerol (TAG) esterification, and the cow's limited ability to export TAG within very low density lipoproteins (VLDL). These hallmark metabolic features of the periparturient period increase a cow's risk of obtaining a postpartum metabolic disease, and can elicit long-term consequences including immunosuppression, compromised milk production, infertility, and reduced longevity. Therefore, it is imperative that we renew our commitment to innovate and develop practical approaches that improve peripartal health. To achieve this goal, we must employ a translational dairy science approach that focuses on characterizing the biochemical mechanisms of insulin resistance and fatty liver, while simultaneously developing practical nutritional strategies that are purposefully designed to target these mechanisms. A systems-biology approach that will help us achieve this goal is the application of mass spectrometry-based lipidomics.
机译：乳制品中的产后代谢疾病涉及脂肪组织胰岛素抵抗和肝脂肪含量的发展。尽管接受了这些代谢器官之间的不利相互作用，但是胰岛素作用和脂肪变性受损的细胞机制并不完全理解。实际上，早期哺乳期胰岛素抵抗促进脂肪组织脂肪解脂肪分解，血脂血症增加了脂肪酸（FA）的肝脏吸收。因此，由于线粒体p氧化，增强的三酰基甘油（标签）酯化和牛在非常低密度脂蛋白（VLDL）内出口标签的有限能力，因此由于线粒体的p氧化，增强的三酰基甘油（标签）酯化能力有限而发展。这些标志性的围类时间段的代谢特征增加了母牛获得产后代谢疾病的风险，并且可以引起长期后果，包括免疫抑制，受损牛奶生产，不孕症和降低寿命。因此，我们必须更新我们的致力于创新和制定改善围属健康的实用方法。为实现这一目标，我们必须采用翻译乳制品科学方法，专注于表征胰岛素抵抗和脂肪肝的生化机制，同时开发实用的营养策略，目的是旨在瞄准这些机制的实用营养策略。一种有助于我们实现这一目标的系统 - 生物学方法是施用基于质谱的脂多种族菌。

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