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首页> 外文期刊>Journal of pediatric endocrinology & metabolism: JPEM >Arginine-guanidinoacetate-creatine pathway in preterm newborns: Creatine biosynthesis in newborns
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Arginine-guanidinoacetate-creatine pathway in preterm newborns: Creatine biosynthesis in newborns

机译:早产新生儿的精氨酸-胍基乙酸盐-肌酸途径:新生儿的肌酸生物合成

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The phosphocreatine/creatine system is fundamental for the proper development of the embryonic brain. Being born prematurely might alter the creatine biosynthesis pathway, in turn affecting creatine supply to the developing brain. We enrolled 53 preterm and very preterm infants and 55 full-term newborns. The levels of urinary guanidinoacetate, creatine, creatinine and amino acids were measured in the preterm and very preterm groups, 48 h and 9 days after birth and at discharge, and 48 h after birth in the full-term group. Guanidinoacetate concentrations of both preterm and very preterm newborns were significantly higher at discharge than the values for the full-term group at 48 h, while very preterm infants showed urinary creatine values significantly lower than those measured in the full-term group. Our results suggest an impairment of the creatine biosynthesis pathway in preterm and very preterm newborns, which could lead to creatine depletion affecting the neurological outcome in prematurely born infants.
机译:磷酸肌酸/肌酸系统对于胚胎大脑的正常发育至关重要。早产可能会改变肌酸的生物合成途径,进而影响向发育中的大脑的肌酸供应。我们招募了53名早产儿和非常早产儿以及55名足月新生儿。在早产组和非常早产组,出生后48 h和9天以及出院时以及足月组中出生48 h后测量尿中鸟嘌呤乙酸盐,肌酸,肌酐和氨基酸的水平。在出院时,早产儿和早产儿的鸟嘌呤乙酸盐浓度在48 h时均显着高于足月组,而早产儿的尿肌酸值则明显低于足月组。我们的结果表明早产儿和非常早产儿的肌酸生物合成途径受到损害,这可能导致肌酸耗竭,影响早产儿的神经功能。

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