Is GAD2 on Chromosome 10p12 a Potential Candidate Gene for Morbid Obesity?

Authors

  • Hemant K. Tiwari PhD,

    Corresponding author
    1. Department of Biostatistics, Section on Statistical Genetics, and the Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama, Birmingham
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  • Luigi Bouchard PhD,

    1. Department of Social and Preventive Medicine, Division of Kinesiology, Laval University, Sainte-Foy, Quebec, Canada
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  • Louis Perusse PhD,

    1. Department of Social and Preventive Medicine, Division of Kinesiology, Laval University, Sainte-Foy, Quebec, Canada
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  • David B. Allison PhD

    1. Department of Biostatistics, Section on Statistical Genetics, and the Clinical Nutrition Research Center, Department of Nutrition Sciences, University of Alabama, Birmingham
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Section on Statistical Genetics, Department of Biostatistics, Ryals Public Health Building, Suite 327, University of Alabama at Birmingham, 1665 University Boulevard, Birmingham, AL 35294; Phone: 205–934–4907; Fax: 205–975–2540; E-mail: htiwari@UAB.edu

Abstract

Morbidly obese individuals represent one of the fastest growing subpopulations of obese individuals. Thus, it is of significant interest to broaden our understanding of the potential genetic causes of this public health concern. A recent study investigated a role of positional candidate gene GAD2 (the gene for glutamic acid decarboxylase) in the development of morbid obesity. This commentary carefully examines the genetic and functional arguments for and against the GAD2 gene as an influential gene for obesity. Also discussed are additional research questions that merit inquiry when further evaluating this genetic variant as a putative contributor to human obesity.

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