Absence of the wild-type allele (192 base pairs) of a polymorphism in the promoter region of the IGF-I gene but not a polymorphism in the insulin gene variable number of tandem repeat locus is associated with accelerated weight gain in infancy

Pediatrics. 2006 Dec;118(6):2374-9. doi: 10.1542/peds.2006-0146.

Abstract

Objective: Our goal was to investigate whether a polymorphism in the insulin-like growth factor I promoter gene (IGF-I, wild-type, 192 base pairs) and in the insulin gene (INS) variable number of tandem repeat locus influence birth weight and weight gain in infancy.

Patients and methods: We obtained genomic DNA from 768 children. Exclusion criteria were multiple births, gestational diabetes, maternal diabetes, gestational age <37 weeks, >42 weeks, or unclear, and any condition potentially influencing weight gain. SD scores were calculated and adjusted for gestational age and gender. A gain in SD scores for weight between birth and 1 year >0.67 SD scores was defined as accelerated weight gain. Genotyping was performed by fragment length analysis (IGF-I) and by fragment length analysis after using a restriction enzyme-based assay (INS variable number tandem repeat).

Results: Accelerated weight gain was present in 205 of 768 children. IGF-I and INS variable number tandem repeat genotype were not associated with birth weight. The IGF-I 192-base pair allele was less frequent in children with accelerated weight gain and was shown to reduce the risk for accelerated weight gain in a logistic regression model.

Conclusion: The IGF-I 192-base pair allele may reduce the risk for rapid weight gain in early infancy.

MeSH terms

  • Alleles
  • Child
  • Child, Preschool
  • Female
  • Humans
  • Insulin / genetics*
  • Insulin-Like Growth Factor I / genetics*
  • Male
  • Minisatellite Repeats / genetics*
  • Polymorphism, Genetic*
  • Time Factors
  • Weight Gain / genetics*

Substances

  • Insulin
  • Insulin-Like Growth Factor I