Single gene mutations causing SGA

Best Pract Res Clin Endocrinol Metab. 2008 Jun;22(3):433-46. doi: 10.1016/j.beem.2008.02.001.

Abstract

The growth hormone-insulin-like growth factor-I (GH-IGF-I) axis plays a key role in intra-uterine growth and development. This review will describe the consequences of genetic defects in various components of the GH-IGF-I axis on intra-uterine growth and development. Animal knockout experiments have provided evidence for the GH-independent secretion of IGF-I and its effect in utero. Reports of patients with a deletion or mutation of the IGF-I and IGF1R genes have provided insight into the role of intra-uterine IGF-I in the human. Homozygous defects of the IGF-I gene have dramatic effects on intra-uterine growth and development, whereas heterozygous defects of the IGF1R gene have a more variable clinical presentation. The phenotype in relation to the genotype of the different disorders will be reviewed in this chapter.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain / growth & development
  • Brain Stem / growth & development
  • Consanguinity
  • Female
  • Fetal Growth Retardation / diagnosis
  • Fetal Growth Retardation / genetics
  • Growth Disorders / diagnosis
  • Growth Disorders / genetics
  • Growth Hormone / genetics*
  • Growth Hormone / physiology
  • Humans
  • Infant, Newborn
  • Infant, Small for Gestational Age*
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Like Growth Factor Binding Proteins / physiology
  • Insulin-Like Growth Factor I / genetics*
  • Male
  • Mice
  • Mice, Knockout
  • Mutation*
  • Pregnancy
  • Receptors, Somatotropin / genetics
  • Receptors, Somatotropin / physiology
  • Signal Transduction

Substances

  • Insulin
  • Insulin-Like Growth Factor Binding Proteins
  • Receptors, Somatotropin
  • Insulin-Like Growth Factor I
  • Growth Hormone