Obese children with low birth weight demonstrate impaired beta-cell function during oral glucose tolerance test

Claudia Brufani1, Armando Grossi, Danilo Fintini

  • 1Bambino Gesù Children's Hospital-Istituto di Ricovero e Cura a Carattere Scientifico, 00165 Rome, Italy. cbrufani@libero.it

Insights

Children born small for gestational age (SGA) who are obese struggle with insulin resistance and beta-cell dysfunction. This leads to poorer glucose control and adverse metabolic outcomes compared to other groups.

Area of Science:

  • Pediatric Endocrinology
  • Metabolic Health
  • Diabetes Research

Background:

  • Birth weight is linked to type 2 diabetes risk.
  • Both small for gestational age (SGA) and large for gestational age (LGA) newborns face increased future diabetes risk.
  • The impact of birth weight on metabolic function in obese children requires further investigation.

Purpose of the Study:

  • To examine how birth weight influences insulin sensitivity and beta-cell function in obese children.
  • To compare metabolic responses among obese children categorized as SGA, appropriate for gestational age (AGA), and LGA.
  • To understand the specific mechanisms linking birth weight to metabolic dysfunction in pediatric obesity.

Main Methods:

  • 257 obese/overweight children (aged 11.6 ± 2.3 yr) were grouped by birth weight percentile: SGA (n=44), AGA (n=161), and LGA (n=52).
  • A 3-hour oral glucose tolerance test (OGTT) was performed with measurements of glucose, insulin, and C-peptide.
  • Insulin sensitivity and beta-cell function were assessed using HOMA-IR, insulinogenic index, disposition index, and glucose/insulin AUC.

Main Results:

  • SGA and LGA children exhibited higher insulin resistance (HOMA-IR) than AGA children.
  • SGA subjects showed elevated glucose AUC and reduced insulinogenic and disposition indexes during OGTT.
  • While overall insulin AUC did not differ, SGA children had lower early (30 min) and higher late (180 min) insulin responses.

Conclusions:

  • Obese children born SGA demonstrate impaired compensatory mechanisms for insulin resistance.
  • Deficits in early insulin secretion and reduced disposition index contribute to higher glucose AUC in SGA children.
  • SGA obese children experience adverse metabolic outcomes, including poorer glucose regulation, compared to AGA and LGA peers.
Abstract

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