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首页> 外文期刊>Pediatrics: Official Publication of the American Academy of Pediatrics >Both relative insulin resistance and defective islet beta-cell processing of proinsulin are responsible for transient hyperglycemia in extremely preterm infants.
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Both relative insulin resistance and defective islet beta-cell processing of proinsulin are responsible for transient hyperglycemia in extremely preterm infants.

机译:相对胰岛素抵抗和胰岛素原的胰岛β细胞加工缺陷都是极早产儿短暂性高血糖的原因。

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摘要

OBJECTIVE: Many extremely preterm infants develop hyperglycemia in the first week of life during continuous glucose infusion. The objective of this study was to determine whether defective insulin secretion or resistance to insulin was the primary factor involved in transient hyperglycemia of extremely preterm infants. METHODS: A prospective comparative study was conducted in appropriate-for-gestational-age preterm infants <30 weeks of gestational age with the aim specifically to evaluate the serum levels of proinsulin, insulin, and C-peptide secreted during transient hyperglycemia by specific immunoassays. Three groups of infants were investigated hyperglycemic (n = 15) and normoglycemic preterm neonates (n = 12) and normal, term neonates (n = 21). In addition, the changes in beta-cell peptide levels were analyzed during and after intravenous insulin infusion in the hyperglycemic group. Data were analyzed using analysis of variance and analysis of variance for repeated measures. RESULTS: At inclusion, insulin and C-peptide levels did not differ in hyperglycemic subjects and in preterm controls. Proinsulin concentration was significantly higher in the hyperglycemic group (36.5 +/- 3.9 vs 23.2 +/- 0.9 pmol/L). Compared with term neonates, proinsulin and C-peptide levels were higher in normoglycemic preterm infants (23.2 +/- 0.9 vs 18.9 +/- 2.71 pmol/L and 1.67 +/- 0.3 vs 0.62 +/- 0.12 nmol/L, respectively). During and after insulin infusion in hyperglycemic neonates, plasma glucose concentration fell and proinsulin and C-peptide levels were lowered (18.4 +/- 7.6 and 20.7 +/- 4.5 pmol/L, respectively). CONCLUSION: These data suggest that 1) preterm neonates are sensitive to changes in plasma glucose concentration, but proinsulin processing to insulin is partially defective in hyperglycemic preterm neonates; 2) hyperglycemic neonates are relatively resistant to insulin because higher insulin levels are needed to achieve euglycemia in this group compared with normoglycemic neonates. These results also show that insulin infusion is beneficial in extremely preterm infants with transient hyperglycemia.
机译:目的:许多极早产婴儿在连续输注葡萄糖的过程中,在出生后的第一周就会出现高血糖。这项研究的目的是确定胰岛素分泌不足或对胰岛素的抵抗是否是极早产儿短暂性高血糖的主要因素。方法:对年龄小于30周的适合胎龄早产儿进行了一项前瞻性比较研究,目的是通过特异性免疫测定来专门评估短暂高血糖过程中分泌的胰岛素原,胰岛素和C肽的血清水平。对三组婴儿进行了高血糖(n = 15)和血糖正常的早产儿(n = 12)和正常足月新生儿(n = 21)的研究。此外,在高血糖组静脉输注胰岛素期间和之后分析了β细胞肽水平的变化。使用方差分析和方差分析对数据进行重复测量。结果:入选时,高血糖受试者和早产对照组的胰岛素和C肽水平没有差异。高血糖组胰岛素原浓度显着较高(36.5 +/- 3.9 vs 23.2 +/- 0.9 pmol / L)。与足月新生儿相比,血糖正常的早产儿的胰岛素原和C肽水平更高(分别为23.2 +/- 0.9 vs 18.9 +/- 2.71 pmol / L和1.67 +/- 0.3 vs 0.62 +/- 0.12 nmol / L) 。在高血糖新生儿中输注胰岛素期间和之后,血浆葡萄糖浓度下降,胰岛素原和C肽水平降低(分别为18.4 +/- 7.6和20.7 +/- 4.5 pmol / L)。结论:这些数据表明:1)早产儿对血浆葡萄糖浓度的变化很敏感,但是高血糖早产儿对胰岛素的原胰岛素加工有部分缺陷; 2)高血糖新生儿相对于胰岛素具有抗性,因为与正常血糖新生儿相比,该组需要更高的胰岛素水平才能实现正常血糖。这些结果还表明,胰岛素输注对于患有短暂高血糖的极早产儿是有益的。

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