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The effects of maternal dietary conjugated linoleic acid on embryonic and post-hatch development in an avian model.

机译:母体饮食中共轭亚油酸对鸟类模型胚胎和孵化后发育的影响。

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摘要

A considerable amount of research has been published on the effects of conjugated linoleic acid (CLA, a group of positional and geometric isomers of 18:2(n-6), added as a 50:50 mixture of cis-9, trans-11 and trans-10, cis-12 CLA) on body and fatty acid composition of growing animals, including mice, rats, pigs, and chicks. Maternal feeding of CLA has been shown to also affect the growth, body composition, and fatty acid profile of tissues in the progeny of mothers fed CLA, possibly through inhibition of enzymes involved in lipid metabolism, such as lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD-1), carnitine 0-palmitoyltransferase (CPT-1), and acyl coenzyme A: cholesterol acyltransferase (ACAT). We have shown that inclusion of 0.5% CLA into a high fat laying hen diet with two types of additional fat sources, safflower oil and olive oil, modulated growth, body composition, and fatty acid profile of three-week-old chicks in comparison to chicks hatched from mothers fed control diets (no CLA). Previous experiments showed that inclusion of CLA into a low-fat laying hen diet resulted in complete loss of hatchability. It has been hypothesized that CLA led to an increase in saturated fatty acids (SFA) and a decrease in monounsaturated fatty acids (MUFA) in the egg yolk as well as surrounding vitelline membrane through inhibition of hen SCD-1. When stored at temperatures below 18°C, the membrane became leaky, which allowed minerals to flow across the membrane down their concentration gradients, and resulted in embryonic mortality in fertile eggs. This phenomenon could be rescued by incorporation of added dietary fat containing high levels of MUFA or polyunsaturated fats. We discovered that in the absence of vitelline membrane disruption (no cooling of eggs prior to incubation) embryos exposed to CLA via maternal diet died. Mortality was not linked to incorporation rate of CLA into the egg yolk fatty acid profile. Mortality in embryos from CLA-fed hens appeared to be linked to the embryo's inability to transport lipid from the yolk sac membrane to the developing embryo in the last week of development resulting in less available energy for tissue growth and maintenance.
机译:关于共轭亚油酸(CLA,一组18:2(n-6)的位置和几何异构体,以50:50顺式9,反式11的混合物添加)的作用已发表了大量研究。和反式10,顺式12 CLA)对正在生长的动物(包括小鼠,大鼠,猪和小鸡)的体内和脂肪酸组成。研究表明,母体喂养CLA还可能通过抑制参与脂类代谢的酶(例如脂蛋白脂肪酶(LPL),硬脂酰-)来影响以CLA喂养的母亲的后代的生长,身体组成和组织的脂肪酸谱。 CoA去饱和酶(SCD-1),肉碱0-棕榈酰转移酶(CPT-1)和酰基辅酶A:胆固醇酰基转移酶(ACAT)。我们已经表明,与三周龄雏鸡相比,高脂蛋鸡日粮中添加了0.5%CLA,其中有两种附加脂肪来源,红花油和橄榄油,调节的生长,身体组成和脂肪酸分布从母亲那里孵出的雏鸡喂饲对照饮食(无CLA)。先前的实验表明,将CLA掺入低脂蛋鸡的饲料中会导致孵化率完全丧失。假设CLA通过抑制母鸡SCD-1导致蛋黄以及卵黄膜周围的饱和脂肪酸(SFA)增加和单不饱和脂肪酸(MUFA)减少。当储存在低于18°C的温度下时,膜会渗漏,使矿物质沿着其浓度梯度向下流过膜,并导致可育卵的胚胎死亡。可以通过添加添加的含有高水平MUFA的饮食脂肪或多不饱和脂肪来挽救这种现象。我们发现,在没有卵黄膜破坏的情况下(在孵化前没有冷却卵),通过母体饮食暴露于CLA的胚胎死亡。死亡率与CLA掺入蛋黄脂肪酸谱中的比率无关。用CLA喂养的母鸡的胚胎死亡率似乎与胚胎在发育的最后一周无法将脂质从卵黄囊膜转运到发育中的胚胎有关,导致组织生长和维持所需的能量减少。

著录项

  • 作者

    Leone, Vanessa Anne.;

  • 作者单位

    The University of Wisconsin - Madison.;

  • 授予单位 The University of Wisconsin - Madison.;
  • 学科 Agriculture Animal Culture and Nutrition.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 197 p.
  • 总页数 197
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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