The study was published online in Nature Genetics and researchers say that the discovery of these genes could lead to tools to predict who is at risk of obesity in childhood. These three genes could be responsible for up to 50% of cases of severe obesity.
Researchers did a genome-wide association study of 1380 European obese children under six and severely obese adults, and 1416 age-matched normal weight controls. Most of the obese adults had been obese since childhood or their teenage years.
The researchers found 38 genetic markers with a strong link to a higher than normal body mass index (BMI). They then investigated these in another 14 186 Europeans and found three mutations that are significantly linked to obesity.
The variant that they found to be most strongly linked with childhood obesity and adult morbid obesity is sited near the PTER gene. Nobody knows what this gene does, but the researchers estimated that the variant probably accounts for up to one third of all childhood obesity and one fifth of all severe adult obesity cases.
The second mutation that was strongly linked to childhood and adult obesity was found in the NPC1 gene, which mouse studies have shown to play a role in appetite control (mice without this gene don't eat much and suffer late-onset weight loss). The researchers estimated that this second variant accounts for about 10% of all childhood obesity and 14% of all cases of severe adult obesity.
The third variant was found near the MAF gene, which controls the making of insulin and glucagon, plus chains of amino acids known as glucagon-like peptides, all of which are important for metabolizing glucose and carbohydrates and in controlling feelings of fullness after eating. The researchers estimated that this variant accounts for about 6 per cent of childhood obesity and 16 per cent of severe adult obesity.
Although the researchers said that more research was needed to see whether these genes are acting independently (it might be the case that they only work together), the joint effect of these new variants could account for up to 50% of all cases of severe adult and childhood obesity.
Researchers hope to develop ways to screen children to find out who is most at risk. This will allow lifestyle modification to prevent obesity occurring.
