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This version published online on October 30, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2007-1822
A more recent version of this article appeared on January 1, 2008
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Submitted on August 14, 2007
Accepted on October 22, 2007

A single nucleotide polymorphism in the p110{beta} gene promoter is associated with partial protection from insulin resistance in severely obese adolescents

Catherine Le Stunff, Agnès Dechartres, Emanuele Miraglia Del Giudice, Philippe Froguel, and Pierre Bougnères*

Pediatric Endocrinology, Pôle d'Endocrinologie Enfants-Adultes Cochin-St Vincent de Paul, APHP, Hôpital Saint Vincent de Paul, Paris V University, Paris, France; INSERM U561, Hôpital Saint Vincent de Paul, Paris, France; Service de Biostatistique et d'Information médicale, Hôpital Necker, Paris, France; Department of Pediatrics, Second University of Naples, Italy; CNRS UMR8090, Pasteur Institute, Lille, France

* To whom correspondence should be addressed. E-mail: pierre.bougneres{at}wanadoo.fr.

Objective. Severe juvenile obesity causes metabolic and cardiovascular complications in adulthood. The catalytic p110{beta} subunit of phosphatidyl-inositol-3 kinase (PI3K) is a major effector of insulin action. We studied the p110{beta} gene as a candidate gene for association with insulin resistance (IR) and fasting glycaemia in severely obese children.

Methods. We conducted an association study in 580 severely obese European children (body mass index > 99.6th centile) and 606 non-obese control children, in whom glucose and insulin were measured in the fasting state. The HOMA-IR index was used to estimate IR.

Results. We found that a single nucleotide polymorphism (rs361072) located in the promoter of the p110{beta} gene was associated with fasting glucose (P=0.0002), insulin (P=2.6 10-8), and HOMA-IR (P=1 10-9) in the severely obese children. The effect of rs361072 was marginal or not significant in non-obese children .

Conclusions. The C allele of rs361072 attenuates IR in superobese children.






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