The −30G>A Polymorphism of the Glucokinase Gene Promoter Is Associated With Obesity in a Population From Southern Spain

Authors

  • Juan M. Gómez-Zumaquero,

    Corresponding author
    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • G. Rojo-Martínez,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • E. García-Escobar,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • Gracia M. Martín-Nuñez,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • J. Haro,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • I. Esteva,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • M. Ruiz de Adana,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • Antonio L. Cuesta,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • G. Olveira,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • S. Morcillo,

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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  • F. Soriguer

    1. Servicio de Endocrinología y Nutrición, Hospital Regional Universitario Carlos Haya (Hospital Civil)-Fundación IMABIS, Málaga, Spain
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(juanm.gomez.exts@juntadeandalucia.es)

Abstract

The aim of this study was to test the hypothesis of an association between the −30G>A polymorphism of the promoter of the glucokinase gene and the prevalence and incidence of obesity. We studied the −30G>A polymorphism of the glucokinase gene promoter in 981 persons, of whom 866 were seen again 6 years later. All the persons underwent an oral glucose-tolerance test and the BMI (weight/height2) was recorded. The −30G>A polymorphism of the glucokinase gene promoter was studied using RFLP-PCR. At the initial study, the probability of having a BMI ≥25 in carriers of the A allele was significantly lower than expected by chance (odds ratio (OR) = 0.63; 95% confidence interval (CI) = 0.456–0.885). In those persons with a BMI ≥30 at the first study, the probability at 6 years of losing weight (reaching a BMI < 30) was greater in carriers of the A allele (OR = 0.22; 95% CI = 0.087–0.576). The increase in weight over these 6 years, taken as a continuous variable, was significantly less only in those persons who were originally obese (P = 0.018). In conclusion, in a population from southern Spain, carriers of the A allele of the −30G>A polymorphism in the promoter of the glucokinase gene had a lower risk for obesity and the likelihood of losing weight was greater in those obese persons who had the A allele (GA or AA).

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