Obesity has increasingly received public attention for being a major health issue in modern societies. In 2010, more than one third of children and adolescents were overweight or obese. Genes, environment, and behavior all contribute to developing obesity. Now, researchers have identified four genes associated with severe childhood obesity and an increased burden of rare structural variations in severely obese children.
The researchers found that structural variations can delete sections of DNA that help to maintain protein receptors known to be linked in the regulation of weight. They believe that these receptors could be targets for the development of new drugs against obesity.
Children with a severe case of obesity are more likely to have a strong genetic contribution. The study is enhancing the understanding of how common and rare variants around certain types of genes 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 BMI, obesity and other obesity-related traits. 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,” Dr. Eleanor Wheeler, first author from the Wellcome Trust Sanger Institute, was quoted as saying.
The results showed that different genes can be associated with in severe childhood obesity compared to obesity in adults. Rare genetic changes in LEPR, one of the newly associated genes, cause a severe fomr of early onset obesity. A more common variant in this gene was identified. It was found in six percent of the population.
Some children involved in the study had an increased number of structural variations of their DNA that delete G-protein coupled receptors, which are important in regulating weight. They are key targets for drug development and may have therapeutic implications for obesity.
“Some children will be obese because they have severe mutations, but our research indicates that some may have a combination of severe mutations and milder acting variants that in combination contribute to their obesity. As we uncover more and more variants and genetic links, we will gain a better basic understanding of obesity, which in turn will open doors to areas of clinically relevant research,” Sadaf Farooqi, co-lead author and professor at the University of Cambridge, was quoted as saying.
The UK10K project team is now exploring all the genes of 1,000 children with severe obesity who have not had a diagnostic mutation found.
“Our study adds evidence that a range of both rare and common genetic variants are responsible for severe childhood obesity,” Dr In?s Barroso, co-lead author from the Wellcome Trust Sanger Institute, was quoted as saying, “This work brings us a step closer to understanding the biology underlying this severe form of childhood obesity and providing a potential diagnosis to the children and their parents.”
SOURCE: University of Cambridge and Wellcome Trust Sanger Institute