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首页> 外文期刊>The Journal of Nutrition: Official Organ of the American Institute of Nutrition >Neonatal Dietary Zinc Deficiency in Artificially Reared Rat Pups Retards Behavioral Development and Interacts with Essential Fatty Acid Deficiency to Alter Liver and Brain Fatty Acid Composition
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Neonatal Dietary Zinc Deficiency in Artificially Reared Rat Pups Retards Behavioral Development and Interacts with Essential Fatty Acid Deficiency to Alter Liver and Brain Fatty Acid Composition

机译：人工饲养大鼠幼崽的新生儿饮食锌缺乏症阻碍行为发展并与必需脂肪酸缺乏症发生相互作用以改变肝脏和脑部脂肪酸组成

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The objective of this study was to investigate whether short-term zinc deficiency in the early neonatal period would exacerbate the effects of essential fatty acid (EFA) deficiency on liver and brain long-chain polyunsaturated fatty acid (LCPUFA) composition, as well as on behavioral development in artificially reared rat pups. Using a 2 × 2 factorial design, male Long-Evans rat pups were reared artificially from postnatal d 5 to 16; pups were fed through gastrostomy tubes with rat formula deficient in zinc and/or EFA. As expected, EFA deficiency significantly reduced levels of arachidonic acid [AA, 20:4(n-6)] and docosahexanoic acid [DHA, 22:6(n-3)] in liver phosphatidylcholine (PC) and brain phosphaditylethanolamine (PE), and increased 22:5(n-6) levels in liver and brain PC and PE. There were significant interactions between zinc and EFA in liver such that zinc deficiency reduced AA and DHA in the EFA-adequate groups, but significantly increased AA in the EFA-deficient groups. Contrary to the hypothesis, short-term zinc deficiency did not exacerbate the effects of EFA deficiency in liver phospholipids. In brain PE, a significant interaction between EFA and zinc was observed such that zinc deficiency increased 22:5(n-6) concentrations in EFA-adequate but not in EFA-deficient groups. Regardless of their EFA status, zinc-deficient rats were growth retarded and demonstrated deficits in locomotor skills. Possible effects of long-term zinc and EFA deficiency on brain function should be investigated in future studies.
机译：这项研究的目的是调查新生儿早期的短期锌缺乏症是否会加剧必需脂肪酸（EFA）缺乏症对肝脏和大脑长链多不饱和脂肪酸（LCPUFA）组成以及对人工饲养的幼仔的行为发展。使用2×2析因设计，从出生后第5天到16天人工饲养雄性Long-Evans大鼠幼崽;幼犬通过胃造口管喂食锌和/或EFA不足的大鼠配方奶。如预期的那样，EFA缺乏显着降低了肝磷脂酰胆碱（PC）和脑磷脂酰乙醇胺（PE）中花生四烯酸[AA，20：4（n-6）]和二十二碳六烯酸[DHA，22：6（n-3）]的水平，并增加了肝脏和大脑PC和PE中22：5（n-6）的水平。锌与肝脏中的EFA之间存在显着的相互作用，因此锌缺乏会降低EFA充足组中的AA和DHA，而在EFA缺乏组中则显着增加AA。与该假设相反，短期锌缺乏并未加剧肝磷脂中EFA缺乏的影响。在大脑PE中，观察到EFA与锌之间的显着相互作用，以致在缺乏EFA的人群中锌缺乏增加了22：5（n-6）的浓度，而在缺乏EFA的人群中没有。不论其EFA状态如何，缺锌大鼠均会发育迟缓并表现出运动技能缺陷。长期锌和EFA缺乏对脑功能的可能影响应在以后的研究中进行研究。

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