Open Access Research article

Analysis of sequence variations in the suppressor of cytokine signaling (SOCS)-3 gene in extremely obese children and adolescents

Katja Hölter1, Anne-Kathrin Wermter1, André Scherag2, Wolfgang Siegfried3, Hanspeter Goldschmidt4, Johannes Hebebrand5 and Anke Hinney5*

Author Affiliations

1 Clinical Research Group, Department of Child and Adolescent Psychiatry, Philipps-University of Marburg, Germany

2 Institute of Medical Biometry and Epidemiology, Philipps-University of Marburg, Germany

3 Obesity Treatment Center Insula, Berchtesgaden, Germany

4 Spessart Klinik, Bad Orb, Germany

5 Department of Child and Adolescent Psychiatry, University of Duisburg-Essen, Essen, Germany

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BMC Medical Genetics 2007, 8:21  doi:10.1186/1471-2350-8-21

Published: 19 April 2007

Abstract

Background

The suppressor of cytokine signaling (SOCS)-3 is a negative feedback regulator of cytokine signaling and also influences leptin signaling. We investigated association of variations in the coding sequence and promoter region of SOCS3 with extreme obesity in German children and adolescents.

Methods

An initial screen for sequence variations in 181 extremely obese children and adolescents and 188 healthy underweight adults revealed two previously reported single nucleotide polymorphisms (SNPs) in the SOCS3 5' region: -1044 C>A (numbering refers to bases upstream of ATG in exon 2) within a predicted STAT3 binding element and -920 C>A (rs12953258, for numbering, see above).

Results

We did not detect significant differences in allele or genotype frequencies for any of these SNPs between the analysed study groups (all nominal p > 0.2). In addition, we performed a pedigree transmission disequilibrium test (PDT) for the SNP -1044 C>A in families comprising 703 obese children and adolescents, 281 of their obese siblings and both biological parents. The PDT revealed no transmission disequilibrium (nominal p > 0.05).

Conclusion

In conclusion, our data do not suggest evidence for a major role of the respective SNPs in SOCS3 in the pathogenesis of extreme obesity in our study groups.