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a The Cardiovascular Institute, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden
Key Words: obesity • visceral fat • abdominal cavity • truncal obesity • gene polymorphism • disease • glucocorticoid receptor gene • obesity • polymorphism • risk
Address for correspondence: Dr. Roland Rosmond, M.D., Ph.D., The Cardiovascular Institute, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden. Voice: +46-31-342-1000; fax: +46-31-826540. e-mail: rolandrosmond{at}hotmail.com
Excess body fat, obesity, is one of the most common disorders in clinical practice. Obese individuals are at increased risk for physical ailments, such as type 2 diabetes, coronary heart disease, hypertension, and several types of cancer. The location of the body fat is a major determinant of the degree of excess morbidity and mortality due to obesity. More specifically, the amount of subcutaneous truncal or abdominal fat, and the amount of visceral fat located in the abdominal cavity independently predicts obesity-related adverse health outcomes. The obesity gene map shows putative loci on all chromosomes except Y. More than 300 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes. These genes can be divided into two broad categories: (a) rare gene variants that have a strong influence, and (b) common gene variants that have a weaker influence on obesity phenotypes. Studies in humans have suggested a positive association between obesity, hypertension, and insulin resistance, with alleles at the glucocorticoid receptor gene. In this article, we will estimate the risk by which such gene polymorphism mediates a role in obesity.
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