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Open Access Commentary

Fat dads must not be blamed for their children's health problems

Gudrun E Moore1* and Philip Stanier2

Author affiliations

1 Clinical and Molecular Genetics Unit, UCL Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK

2 Neural Development Unit, UCL Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK

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Citation and License

BMC Medicine 2013, 11:30  doi:10.1186/1741-7015-11-30

Please see related research article here

Published: 6 February 2013


The relationship between the parental genomes in terms of the future growth and development of their offspring is not critical. For the majority of the genome the tissue-specific gene expression and epigenetic status is shared between the parents equally, with both alleles contributing without parental bias. For a very small number of genes the rules change and control of expression is restricted to a specific, parentally derived allele, a phenomenon known as genomic imprinting. The insulin-like growth factor 2 (Igf2/IGF2) is a robustly imprinted gene, important for fetal growth in both mice and humans. In utero IGF2 exhibits paternal expression, which is controlled by several mechanisms, including the maternally expressing untranslated H19 gene. In the study by Soubry et al., a correlation is drawn between the IGF2 methylation status in fetal cord blood leucocytes, and the obesity status of the father from whom the active IGF2 allele is derived through his sperm. These data imply that paternal obesity affects the normal IGF2 methylation in the sperm and this in turn alters the expression of IGF2 in the baby.

Insulin-like growth factor 2; paternal obesity; DNA methylation; genomic imprinting