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Maternal type 1 and gestational diabetes: postnatal differences in insulin secretion in offspring at preschool age

Jatta Pirkola1, Marja Vääräsmäki, Erja Leinonen

  • 1Department of Obstetrics and Gynaecology, Oulu University Hospital, Oulu, Finland. jatta.pirkola@gmail.com

Pediatric Diabetes
|May 30, 2008
PubMed

Insights

Children exposed to maternal type 1 diabetes (T1DM) or gestational diabetes (GDM) show distinct metabolic changes by preschool age. Maternal weight gain during pregnancy also influences offspring glucose metabolism.

Area of Science:

  • Endocrinology and Metabolism
  • Pediatric Health
  • Reproductive Health

Background:

  • Maternal diabetes in pregnancy (type 1 diabetes mellitus [T1DM] and gestational diabetes mellitus [GDM]) is linked to later metabolic abnormalities in offspring.
  • Previous research often did not distinguish between T1DM and GDM offspring or lacked adequate control groups.

Purpose of the Study:

  • To compare insulin secretion and insulin resistance in preschool-aged children born to mothers with T1DM, GDM, and no diabetes.
  • To investigate the long-term metabolic effects of prenatal diabetes exposure.

Main Methods:

  • Study included offspring of mothers with T1DM (n=16), GDM (n=22), and no diabetes (n=25).
  • Intravenous glucose tolerance testing and anthropometric measurements were conducted.
  • Analysis included first-phase insulin response (FPIR) and HOMA values, with statistical analysis using ANOVA and ANCOVA.

Main Results:

  • Offspring of mothers with T1DM exhibited higher fasting insulin, FPIR, and HOMA-B values compared to GDM and control groups (p < 0.05).
  • No significant differences were observed between groups when adjusted for maternal weight gain during pregnancy.
  • GDM pregnancies were associated with the least maternal weight gain.

Conclusions:

  • Prenatal exposure to T1DM and GDM may differentially impact offspring glucose metabolism by age 5.
  • Maternal weight gain during pregnancy is a significant factor influencing postnatal glucose metabolism in offspring.
Abstract

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