Related Experiment Video
Updated: Apr 5, 2026

Isolation, Culture, and Imaging of Human Fetal Pancreatic Cell Clusters
Published on: May 18, 2014
A C-Peptide-Based Model of Pancreatic Insulin Secretion in Extremely Preterm Neonates in Intensive Care
Jennifer L Dickson1, Jane Alsweiler2, Cameron A Gunn3
1Department of Mechanical Engineering, University of Canterbury, Christchurch, New Zealand jennifer.dickson@canterbury.ac.nz.
Insights
This study developed a sex-based model for infant insulin secretion to improve model-based glycemic control in neonatal intensive care. Infant insulin secretion is complex and not predictable by nutritional intake alone.
Area of Science:
- Neonatal physiology
- Endocrinology
- Computational biology
Background:
- Model-based glycemic control requires accurate patient physiology models.
- Infant glucose-insulin metabolism differs from adults and is understudied.
- C-peptide analysis aids in developing insulin secretion models for neonatal intensive care.
Purpose of the Study:
- To develop and validate insulin secretion models for very preterm infants.
- To improve model-based glycemic control strategies in neonatal intensive care.
- To investigate factors influencing insulin secretion in this population.
Main Methods:
- Retrospective analysis of plasma C-peptide, insulin, and blood glucose concentrations in 41 hyperglycemic very preterm infants.
- Utilized a 2-compartment model of C-peptide kinetics to estimate insulin secretion.
- Examined insulin secretion in relation to nutritional intake, exogenous insulin, and blood glucose levels.
Main Results:
- Insulin secretion demonstrated high inter-patient and intra-patient variability.
- Nutritional intake (protein, dextrose) did not reliably predict insulin secretion.
- Insulin secretion increased with blood glucose, with a stronger correlation observed in female infants.
Conclusions:
- A sex-based insulin secretion model was successfully developed for glycemic control frameworks.
- Nutritional intake is not a sole determinant of insulin secretion in very preterm infants.
- Insulin secretion is influenced by a complex interplay of metabolic factors.
Background:
Model-based glycemic control relies on sufficiency of underlying models to describe underlying patient physiology. In particular, very preterm infant glucose-insulin metabolism can differ significantly from adults, and is relatively unstudied. In this study, C-peptide concentrations are used to develop insulin-secretion models for the purposes of glycemic control in neonatal intensive care.
Methods:
Plasma C-peptide, insulin, and blood glucose concentrations (BGC) were retrospectively analyzed from a cohort of 41 hyperglycemic very preterm (median age 27.2 [26.2-28.7] weeks) and very low birth-weight infants (median birth weight 839 [735-1000] g). A 2-compartment model of C-peptide kinetics was used to estimate insulin secretion. Insulin secretion was examined with respect to nutritional intake, exogenous and plasma insulin concentration, and BGC.
Results:
Insulin secretion was found to be highly variable between patients and over time, and could not be modeled with respect to age, weight, or protein or dextrose intake. In 13 of 54 samples exogenous insulin was being administered, and insulin secretion was lower. However, low data numbers make this result inconclusive. Insulin secretion was found to increase with BG, with a stronger association in female infants than males (R(2) = .51 vs R(2) = .13, and R(2) = .26 for the combined cohort).
Conclusions:
A sex-based insulin secretion model was created and incorporated into a model-based glycemic control framework. Nutritional intake did not predict insulin secretion, indicating that insulin secretion is a complex function of a number of metabolic factors.
Related Concept Videos
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
Insulin and C-peptide are...
Insulin Secretory Vesicles
Insulin: Biosynthesis, Chemistry, and Preparation
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
Cell Specific Gene Expression

