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Maternal and fetal genetic predispositions to insulin deficiency and resistance affect fetal growth through distinct

Gechang Yu1,2,3, Claudia H T Tam1,2,3, Mai Shi1,2,3

  • 1Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.

Diabetologia
|February 3, 2026
PubMed

Insights

Maternal and fetal genetic risks for type 2 diabetes impact offspring growth differently. Targeting maternal hyperglycemia and BMI may reduce large-for-gestational-age births.

Area of Science:

  • Genetics
  • Metabolic Health
  • Perinatal Medicine

Background:

  • Maternal and fetal genetic factors influence fetal growth.
  • Insulin resistance and deficiency are key in type 2 diabetes (T2D) and impact metabolic health.
  • Distinct pathways may mediate these genetic effects on fetal development.

Purpose of the Study:

  • To investigate if maternal and fetal genetic predispositions for insulin deficiency and resistance affect offspring fetal growth via separate pathways.
  • To analyze these associations across multi-ethnic populations.

Main Methods:

  • Examined associations of maternal and fetal partitioned polygenic risk scores (pPRSs) for T2D-related pathways with fetal growth outcomes (birthweight, SSF, LGA, SGA) in 5065 mother-infant pairs.
  • Utilized two-sample Mendelian randomisation (2SMR) in Europeans for triangulation.
  • Employed mediation analysis for maternal glucose/BMI and cord C-peptide effects, and co-localisation analyses for shared causal variants.

Main Results:

  • Fetal T2D PRS and pPRSs for lipodystrophy/impaired fasting glucose (IFG) were linked to lower birthweight/SSF.
  • Maternal T2D PRS and pPRSs for IFG/obesity were linked to higher birthweight/SSF/LGA, consistent across ethnicities.
  • Maternal hyperglycemia and BMI significantly mediated these maternal genetic effects; 2SMR confirmed findings and linked fetal insulin sensitivity to higher birthweight.

Conclusions:

  • Reduced fetal growth may stem from lipodystrophy-related insulin resistance and IFG-related insulin deficiency pathways.
  • Interventions targeting pregnant women with high T2D PRS/pPRS, focusing on reducing post-load hyperglycemia and BMI, could mitigate offspring LGA risk.
Abstract

Keywords:
Fetal growthInsulin deficiencyInsulin resistanceMendelian randomisationMulti-ethnic populationsPartitioned polygenic risk scoresType 2 diabetes

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