Some people are able to tuck into chocolate every day and not gain weight, while others struggle to keep their weight down regardless of what they eat. Exactly why this is has been unclear, but now researchers point to a genetic mutation as the cause.
Researchers from the University of Cambridge in the UK say that mutation of a gene called KSR2 may cause continued hunger pangs in patients who are obese, as well as slow their metabolism – the rate at which the body burns calories.
These findings could provide some explanation for the increase in childhood obesity. According to the
Previous studies have demonstrated that deleting the KSR2 gene in mice caused them to develop obesity. This highlighted KSR2 as an important factor in regulating energy balance and metabolism.
But until now, it has been unclear as to whether this gene has the same effect in human subjects.
To reach their findings, published in the journal Cell, the researchers analyzed the genetic sequences of 2,101 children suffering from early-onset obesity, and compared these with the sequences of children of a normal, healthy weight.
Results of the analysis revealed that children who showed a mutation in the KSR2 gene demonstrated an increased appetite, slower metabolism, lower heart rate and severe insulin resistance compared with those who had a normal version of the gene.
Further experiments in cells also revealed that KSR2 mutations impaired metabolic processes, such as glucose and fatty acid oxidation.
Sadaf Farooqi of the University of Cambridge and study author, explains that although changes in diet and levels of physical activity underlie the recent increase in obesity, their findings show that some people do gain weight more easily than others.
“This variation between people is largely influenced by genetic factors. The discovery of a new obesity gene, KSR2, demonstrates that genes can contribute to obesity by reducing metabolic rate – how well the body burns calories.”
The researchers note that these findings indicate that drugs could be developed for new treatment options for obesity and type 2 diabetes, by regulating the protein that is encoded by the KSR2 gene.
Through conducting experiments with metformin – a drug used to treat diabetes – the researchers found that it increased the low levels of fatty oxidation in cells with KSR2 mutations.
“These observations and our in vitro ﬁndings suggest that pharmacological approaches based on the modulation of KSR2 activity could represent a novel potential therapeutic strategy for the treatment of obesity and type 2 diabetes,” the researchers say.
They add that further studies are warranted to determine exactly to what extent metformin can alleviate the effects of KSR2 mutation.
Medical News Today recently reported on a study suggesting that women who gain excessive weight during pregnancy are at risk of having obese children.