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<b><i>Background:</i></b> Fetal growth failure has been associated with an increased risk of hypertension, cardiovascular disease and diabetes in adulthood. Exploring the mechanisms underlying this association should improve our understanding of these common adult diseases. <b><i>Patients and Methods:</i></b> We investigated 225 SNPs in 10 genes involved in growth and glucose metabolism (<i>GH1, GHR, IGF1, IGF1R, STAT5A, STAT5B, MAPK1, MAPK3, PPAR&#947; </i>and<i> INS</i>) in 1,437 children from the multinational NESTEGG consortium: 345 patients born small for gestational age who remained short (SGA-S), 288 who showed catch-up growth (SGA-Cu), 410 idiopathic short stature (ISS) and 394 controls. We related genotype to pre- and/or postnatal growth parameters, response to growth hormone (if applicable) and blood pressure. <b><i>Results:</i></b> We found several clinical associations for <i>GH1, GHR, IGF1, IGF1R, PPAR&#947; </i>and <i>MAPK1.</i> One SNP remained significant after Bonferroni's correction: <i>IGF1R</i> SNP rs4966035's minor allele A was significantly more prevalent among SGA and associated with smaller birth length (p = 0.000378) and birth weight (weaker association), independent of gestational age. <b><i>Conclusion:</i></b><i>IGF1R</i> SNP rs4966035 is significantly associated with birth length, independent of gestational age. This and other associations suggest that polymorphisms in these genes might partly explain the phenotype of short children born SGA and children with ISS.

Original publication

DOI

10.1159/000355409

Type

Journal article

Journal

Hormone Research in Paediatrics

Publisher

S. Karger AG

Publication Date

2013

Volume

80

Pages

466 - 476