A new study found that the gene most commonly linked to the development of obesity may be turned off with some tweaks, causing metabolic processes to burn up extra fats.
Obesity has long been associated with increased food consumption and lack of physical activity. However, the role of genetics cannot be disregarded and experts have discovered that genes have a significant contribution to whether fat is stored up in the body or expended as energy. Part of the study is the discovery of a breakthrough technique that is said to have the capability of "turning off" those genes by cutting out the faulty DNA code and mend it with the accurate sequence.
Fat mass and obesity-associated (FTO) protein or the alpha-ketoglutarate-dependent dioxygenase enzyme is the gene that is typically linked to obesity development and high Body Mass Index (BMI). Although, scientists have acknowledged that the FTO regions have the most explicit relationship with obesity, the mechanisms that drove the said association are not clearly identified.
The researchers from the Harvard University and the Massachusetts Institute of Technology (MIT) analyzed genetic data, activity, conservation properties, regulator expressions and coexpression patterns of the gene to find out the mechanistic foundation surrounding the relationship of obesity and the FTO region. The researchers obtained fat samples from European subjects who have the obesity-related gene and those who have just the normal copies.
The findings of the study, published in The New England Journal of Medicine, show that the obesity gene stimulates two other genes to inhibit the process of thermogenesis, which is the mechanism that burns up fat. The researchers used the emergent Crispr/Cas9 system to tweak the DNA code and repair the sequence in the subjects. Replacement of the variant one letter of the DNA code took place and with this, the genes called IRX3 and IRX5, which conserve fat during starvation and other fat loss events, are activated even if they should not.
"Knowing the causal variant underlying the obesity association may allow genome editing as a therapeutic avenue for individuals as risk," said Professor Manolis Kellis, senior author from the MIT's Computer Science and Artificial Intelligence Laboratory (CSAIL) and of the Broad Institute. By making changes in this pathway, experts can now manipulate whether fats are stored or used as energy, which is a good development in the treatment of obesity.
Photo: Mike Licht | Flickr
