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C-Peptide Suppression During Insulin Infusion in the Extremely Preterm Infant Is Associated With Insulin Sensitivity

William Hellström1, Ingrid Hansen-Pupp2, Gunnel Hellgren3,4

  • 1Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

The Journal of Clinical Endocrinology and Metabolism
|May 7, 2019
PubMed

Insights

Exogenous insulin infusion in extremely preterm infants suppressed C-peptide levels individually. Insulin sensitivity influenced this effect, with lower sensitivity causing a greater C-peptide decrease during treatment.

Area of Science:

  • Neonatalogy
  • Endocrinology
  • Metabolic Research

Background:

  • Limited understanding of glucose-regulating factor responses to exogenous insulin in extremely preterm infants.
  • Hyperglycemia is a common issue in extremely preterm infants requiring management.

Purpose of the Study:

  • To evaluate longitudinal serum concentrations of insulin, C-peptide, and plasma glucose.
  • To assess these factors in extremely preterm infants receiving insulin for hyperglycemia using high-frequency sampling.

Main Methods:

  • Prospective longitudinal cohort study in two Swedish university hospitals.
  • Nine extremely preterm infants (22-26 weeks gestation) with hyperglycemia were monitored.
  • Serum samples collected at multiple time points during and after insulin infusion.

Main Results:

  • Serum C-peptide concentrations decreased during insulin infusion and increased post-infusion.
  • Individual insulin sensitivity correlated with the initial and lasting decrease in C-peptide levels.
  • Lower insulin sensitivity was linked to a more pronounced C-peptide suppression.

Conclusions:

  • Exogenous insulin infusion differentially suppresses C-peptide concentrations in extremely preterm infants.
  • The impact of insulin infusion on beta cells appears related to individual insulin sensitivity.
  • Findings suggest a link between insulin sensitivity and beta-cell response during treatment.
Abstract

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