Genetic mutation fuels childhood obesity – Study
Ever wondered why some people can eat just about anything without gaining a pound, while others struggle to cut down their weight despite adopting all weight loss measure.
Well, researchers seem to have found the answer.
Researchers from the University of Cambridge in the UK have discovered a gene mutation, called KSR2, which triggers hunger pangs in obese and overweight patients. The gene, researchers say, is also responsible for slow metabolism, the rate at which the calories in the body are burnt.
Earlier studies had established that deleting the KSR2 gene in mice made them profoundly overweight, highlighting its role in regulating energy balance and metabolism. But whether the gene played the same role in human subjects was unclear.
To check if KSR2 gene was responsible for fuelling human obesity too, researchers analyzed the genetic sequencing in 2,101 children suffering from early-onset obesity.
The findings were compared with genetic sequences of children who were healthy and weighed normal.
Researchers found that children with the gene mutation KSR2 were more likely to have an increased appetite, slower metabolism, lower heart rate and severe insulin resistance as compared to those who did not have the gene.
Furthermore, KSR2 mutations impaired the metabolic processes, like the glucose and fatty acid oxidation, researchers noted.
Explaining why some people gain weight more easily than others, study’s lead researcher, Sadaf Farooqi of the University of Cambridge said, “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.”
Potential treatment for obesity and diabetes
Regulating the protein that is encoded by the KSR2 gene, my well become the basis of new treatment options targeting obesity and type 2 diabetes, researchers say.
“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.
The findings of the study are reported in the current issue of the journal Cell.