Empowering Healthy Kids Blog

10 year research from the Department of Genomic Medicine at Imperial College London found three genetic variants that can go some way to explain the biological reasons for obesity:

The gene variant most strongly associated with childhood obesity and adult morbid obesity in the study is located near the PTER gene, the function of which is not known. This variant is estimated to account for up to a third of all childhood obesity, and a fifth of all cases of adult obesity.

The second variant associated with child and adult obesity is found in the NPC1 gene. Previous studies in mice have suggested that this gene has a role in controlling appetite, as mice with a non-functioning NPC1 gene suffer late-onset weight loss and have poor food intake. This gene variant accounts for around 10 per cent of all childhood obesity and about 14 per cent of adult morbid obesity cases.

The final variant is found near the MAF gene, which controls the production of the hormones insulin and glucagon, as well as chains of amino acids called glucagon-like peptides. These hormones and peptides are known to play key roles in people’s metabolisms by metabolising glucose and carbohydrates in the body. In addition, glucagon and glucagon-like peptides appear to have a strong effect on people’s ability to feel ‘full’ or satiated after eating. This variant accounts for about 6 per cent of early-onset obesity in children, and 16 per cent of adult morbid obesity.

Further research is needed to determine whether the gene variants are acting independently, but if they are, then together these three new variations may account for up to half of all cases of severe adult and child obesity.

This entry (Permalink) was posted on Monday, January 19th, 2009 at 3:49 pm and is filed under genes, uk, research, childhood obesity. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response , or trackback from your own site.