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Associations of maternal CDKAL1 gene with adverse offspring growth patterns

Zhiyi Hao1, Meng Su1, Ming Gao1,2,3

  • 1Department of Epidemiology and Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, China.

Pediatric Research
|July 8, 2026
PubMed

Insights

Maternal CDKAL1 gene is linked to offspring's persistent lean and obesity growth patterns, independent of gestational diabetes mellitus (GDM). This finding highlights a direct genetic influence on childhood growth beyond GDM pathways.

Area of Science:

  • Genetics and Epigenetics
  • Pediatric Endocrinology
  • Maternal-Fetal Medicine

Background:

  • Gestational diabetes mellitus (GDM) is a known risk factor for adverse offspring growth patterns.
  • The role of specific maternal genes, such as CDKAL1, in influencing offspring growth independently of GDM is less understood.

Purpose of the Study:

  • To investigate the association between maternal CDKAL1 gene variants and offspring growth patterns (ages 1-8 years).
  • To determine if GDM mediates the relationship between maternal CDKAL1 and offspring growth.

Main Methods:

  • Longitudinal study of 345 mother-infant pairs in China over 8 years.
  • Group-based trajectory modeling to identify offspring growth patterns.
  • Analysis of CDKAL1 polygenic risk scores (PRS) association with growth patterns using logistic regression and restricted cubic splines, with and without GDM adjustment.

Main Results:

  • Four offspring growth patterns were identified: normal, persistent lean, and obesity (including late-onset and persistent subtypes).
  • Higher CDKAL1 PRS was significantly associated with both persistent lean (OR: 1.91) and obesity (OR: 2.07) growth patterns.
  • These associations remained significant even after adjusting for GDM, indicating an independent genetic effect.

Conclusions:

  • Maternal CDKAL1 gene is independently associated with increased risk for both persistent lean and obesity growth patterns in offspring.
  • This suggests a direct genetic pathway influencing childhood growth, separate from GDM-mediated effects.
  • Findings offer insights into genetic predispositions for childhood growth disparities and potential for early intervention.
Abstract

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