Mericq V
Institute of Maternal and Child Research, Faculty of Medicine, University of Chile, Santiago.
Horm Res. 2006;65 Suppl 3:131-6. doi: 10.1159/000091518. Epub 2006 Apr 10.
Premature infants of low and extremely low birth weight represent a challenge for neonatal intensive care units and paediatricians. These neonates may be at increased risk of insulin resistance and diabetes perinatally and during childhood. During the first week of postnatal life, infants born prematurely are at risk of abnormalities in glucose homeostasis. Additionally, there are major differences in their glucose/insulin homeostasis compared with infants born at term. Preterm infants are at risk of hypoglycaemia, due to decreases in deposits of glycogen and fat that occur during the third trimester, and also to transient hyperinsulinaemia. Hyperglycaemia may also be observed in preterm infants during the perinatal period. These infants are unable to suppress glucose production within a large range of glucose and insulin concentrations, insulin secretory response is inappropriate, insulin processing is immature and there is an increased ratio of the glucose transporters Glut-1/Glut-2 in fetal tissues, which limits sensitivity and hepatocyte reaction to increments in glucose/insulin concentration during hyperglycaemia. In addition, increased concentrations of tumour necrosis factor alpha present in intrauterine growth retardation (IUGR) and induce insulin resistance. It has been proposed that the reduced insulin sensitivity may result from adaptation to an adverse in utero environment during a critical period of development. We have investigated postnatal insulin resistance in 60 children born with very low birth weight and either small for gestational age or at an appropriate size for gestational age. This study showed that IUGR, rather than low birth weight itself, was associated with increased fasting insulin levels. As poor fetal growth may be associated with the development of obesity, type 2 diabetes and the metabolic syndrome in later life, it is important that we continue to increase our understanding of the effects of IUGR on postnatal growth and metabolism.
低出生体重和极低出生体重的早产儿对新生儿重症监护病房和儿科医生来说是一项挑战。这些新生儿在围产期和儿童期可能有更高的胰岛素抵抗和糖尿病风险。在出生后的第一周，早产儿有葡萄糖稳态异常的风险。此外，与足月儿相比，他们的葡萄糖/胰岛素稳态存在重大差异。由于孕晚期糖原和脂肪储备减少以及短暂的高胰岛素血症，早产儿有低血糖风险。围产期也可能在早产儿中观察到高血糖。这些婴儿在大范围的葡萄糖和胰岛素浓度内无法抑制葡萄糖生成，胰岛素分泌反应不适当，胰岛素加工不成熟，并且胎儿组织中葡萄糖转运蛋白Glut-1/Glut-2的比例增加，这限制了高血糖期间对葡萄糖/胰岛素浓度增加的敏感性和肝细胞反应。此外，宫内生长受限（IUGR）中存在的肿瘤坏死因子α浓度增加并诱导胰岛素抵抗。有人提出，胰岛素敏感性降低可能是由于在关键发育时期适应了不利的子宫内环境。我们调查了60名出生时极低出生体重且小于胎龄或适于胎龄的儿童的出生后胰岛素抵抗情况。这项研究表明，宫内生长受限而非低出生体重本身与空腹胰岛素水平升高有关。由于胎儿生长不良可能与晚年肥胖、2型糖尿病和代谢综合征的发生有关，因此继续加深我们对宫内生长受限对出生后生长和代谢影响的理解非常重要。
