Researchers discover new genetic factors in severe obesity
An international team of researchers has identified three genetic variants which increase an individual's risk of becoming obese and may be responsible for up to half of all existing cases of severe obesity. The study, which was funded in part by the EU's Fifth Framework Programme (FP5), is published in the journal Nature Genetics. According to the World Health Organization (WHO), the prevalence of obesity has tripled in many European countries since the 1980s, and the numbers of those affected, particularly children, continue to rise. 'When young children become obese, their lives can be affected in a very negative way,' said Professor Philippe Froguel of France's National Scientific Research Centre (CNRS) and Imperial College London, UK. 'Sadly, obese children are often unfairly stigmatised and they can suffer heart and lung problems, painful joints, diabetes and cancer as they grow up.' In this latest research, scientists conducted a genome-wide association study, which entails examining each study participant's entire genome for 'markers' of genetic variation that might be associated with a particular trait (in this case, obesity). Two groups were compared: 1,380 Europeans with early-onset (before the age of six) childhood obesity and adult morbid obesity, and 1,416 age-matched, normal-weight controls. The genotypes of 14,186 European subjects were also examined; in this group, 38 genetic markers were strongly associated with a higher-than-normal body mass index (a measure of obesity). The findings point to three mutations that are significantly linked to the risk of severe obesity. This represents a great step forward in the search for tools to effectively screen for obesity risk in young children. 'Understanding the genetic basis of obesity is the first step towards helping these children,' said Professor Froguel. 'Once we identify the genes responsible, we can develop ways to screen children to find out who is most at risk of becoming obese. Hopefully we can then intervene with measures such as behavioural therapy, to make sure a child forms healthy eating habits and does not develop a weight problem.' One of the newly discovered genetic variants, located near the mysterious PTER gene, accounted for an estimated third of all childhood-onset obesity and a fifth of all adult obesity cases. Another variant, found in the NPC1 gene (which is implicated in controlling appetite), was estimated to account for up to 10% of all childhood obesity and 14% of adult morbid-obesity cases. Another variant was found near the MAF gene, which among other functions, controls the production of insulin, glucagon and glucagon-like peptides (which have an effect on feelings of satiety). All of these compounds play an important role in sugar and carbohydrate metabolism. The genetic variant was found to be involved in approximately 6% of early-onset childhood obesity and 16% of adult morbid obesity cases. EU support for the research came from the EURO-BLCS ('Biological, clinical and genetic markers of future risk of cardiovascular disease') project, a multinational epidemiological study financed through the 'Quality of life and management of living resources' budget line of FP5.
Countries
Canada, Switzerland, Germany, Finland, France, United Kingdom