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首页> 外文期刊>The Journal of Nutritional Biochemistry >Postnatal growth velocity modulates alterations of proteins involved in metabolism and neuronal plasticity in neonatal hypothalamus in rats born with intrauterine growth restriction.
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Postnatal growth velocity modulates alterations of proteins involved in metabolism and neuronal plasticity in neonatal hypothalamus in rats born with intrauterine growth restriction.

机译：出生后生长速度可调节宫内生长受限的新生鼠下丘脑中参与代谢和神经元可塑性的蛋白质变化。

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Intrauterine growth restriction (IUGR) due to maternal protein restriction is associated in rats with an alteration in hypothalamic centers involved in feeding behaviour. In order to gain insight into the mechanism of perinatal maternal undernutrition in the brain, we used proteomics approach to identify hypothalamic proteins that are altered in their expression following protein restriction in utero. We used an animal model in which restriction of the protein intake of pregnant rats (8% vs. 20%) produces IUGR pups which were randomized to a nursing regimen leading to either rapid or slow catch-up growth. We identified several proteins which allowed, by multivariate analysis, a very good discrimination of the three groups according to their perinatal nutrition. These proteins were related to energy-sensing pathways (Eno 1, E2PDH, Acot 1 and Fabp5), redox status (Bcs 1L, PrdX3 and 14-3-3 protein) or amino acid pathway (Acy1) as well as neurodevelopment (DRPs, MAP2, Snca). In addition, the differential expressions of several key proteins suggested possible shunts towards ketone-body metabolism and lipid oxidation, providing the energy and carbon skeletons necessary to lipogenesis. Our results show that maternal protein deprivation during pregnancy only (IUGR with rapid catch-up growth) or pregnancy and lactation (IUGR with slow postnatal growth) modulates numerous metabolic pathways resulting in alterations of hypothalamic energy supply. As several of these pathways are involved in signalling, it remains to be determined whether hypothalamic proteome adaptation of IUGR rats in response to different postnatal growth rates could also interfere with cerebral plasticity or neuronal maturation.
机译：由于母体蛋白质限制而引起的宫内生长受限（IUGR）与大鼠的下丘脑中心改变有关，与进食行为有关。为了深入了解围产期孕产妇大脑营养不足的机制，我们使用蛋白质组学方法来鉴定下丘脑蛋白，这些蛋白在子宫内进行蛋白质限制后表达改变。我们使用了一种动物模型，其中，限制怀孕大鼠蛋白质摄入量（8％对20％）会产生IUGR幼崽，将其随机分配到导致快速或缓慢追赶性生长的护理方案中。通过多变量分析，我们鉴定了几种蛋白质，根据其围产期营养，可以很好地区分这三组蛋白质。这些蛋白质与能量感应途径（Eno 1，E 2 PDH，Acot 1和Fabp5），氧化还原状态（Bcs 1L，PrdX3和14-3-3蛋白）或氨基酸途径有关。 Acy1）以及神经发育（DRP，MAP2，Snca）。此外，几种关键蛋白的差异表达提示可能会分流至酮体代谢和脂质氧化，从而为脂肪生成提供必要的能量和碳骨架。我们的结果表明，仅在妊娠期间（快速追赶增长的IUGR）或妊娠和哺乳期（出生后增长缓慢的IUGR），母体蛋白质缺乏会调节许多代谢途径，导致下丘脑能量供应的改变。由于这些途径中的几种都参与信号传导，因此有待确定IUGR大鼠的下丘脑蛋白质组适应不同的出生后生长速率是否还会干扰脑可塑性或神经元成熟。

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