Researchers have identified four genes newly associated with severe childhood obesity. They also found an increased burden of rare structural variations in severely obese children. The new work was reported online on April 7, 2013 in Nature Genetics. The research team found that structural variations can delete sections of DNA that help to maintain protein receptors known to be involved in the regulation of weight. These receptors are promising targets for the development of new drugs against obesity. As one of the major health issues affecting modern societies, obesity has increasingly received public attention. Genes, behavior, and environment, all contribute to the development of obesity. Children with severe obesity are more likely to have a strong genetic contribution. This study has enhanced understanding of how both common and rare variants around specific genes and genetic regions are involved in severe childhood obesity. “We’ve known for a long time that changes to our genes can increase our risk of obesity. For example, the gene FTO has been unequivocally associated with body-mass index (BMI), obesity, and other obesity-related traits,” says Dr. Eleanor Wheeler, first author from the Wellcome Trust Sanger Institute. “In our study of severely obese children, we found that variations in or near two of the newly associated genes seem to have a comparable or greater effect on obesity than the FTO gene: PRKCH and RMST.” The team found that different genes can be involved in severe childhood obesity compared to obesity in adults. Rare genetic changes in one of the newly associated genes, LEPR, are known to cause a severe form of early-onset obesity. The team identified a more common variant in this gene, found in 6 per cent of the population, that can increase a person’s risk of obesity.
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