Tweaking DNA Can Help End Obesity Crisis

Tweaking DNA Can Help End Obesity Crisis

TEHRAN (Tasnim) - Researchers say that by tweaking CRISPR, a tool for making edits to DNA, the cells could be changed to prevent people from being tempted by calorific treats and help people who are trying to lose weight in a bid to tackle the obesity crisis.

They are working on a method that will modify the genes of people who are trying to lose weight in a bid to tackle the obesity crisis.

This will be done by using CRISPR-A, a new technique, with the 'A' standing for activation - used to heighten genes that suppress appetite, Daily Mail reported.

The system differs from CRISPR in that it doesn't make cuts to the genome, but amplifies the activities of certain genes.

CRISPR is usually used to remove or 'knock out' a particular gene, but the new technique replaces the 'molecular scissors with a volume control knob'.

The method has the same guidance system as CRISPR, which is used to find a particular DNA sequence but when the version targets the genome, it ramps it up.

Navneet Matharu, who led the study, said that the CRISPR-could potentially provide a cure for obesity and other diseases.

In the case of weight loss, the study said that the researchers were able to achieve long lasting weight control without making a single edit to the genome.

authors of the study, by scientists from the University of California, tested on mice with genetic mutations which make them more likely to gain weight.

They used CRISPR to locate the genetic mutation in the mice that makes them predisposed to gaining weight.

By tweaking the activities of those genes, the result was that these mice were slim.

CRISPR relies on the fact that mammals have two copies of every gene, one from each parent.

There are at least 660 genes where a mutation in one copy appears to be linked to disease.

SIM1 is the gene that plays the role in regulating hunger, mutations of which have been observed in severely overweight patients.

both copies are working, people and mice are able to limit their food intake whereas in other cases the set of genes could have a mutation rendering one copy useless and the other not being able to provide a sufficient feeling of fullness.

'Mice that were missing one copy of the SIM1 gene received the CRISPR-A injections at four weeks of age and maintained a healthy body weight.

Mice that didn't receive CRISPR-A injections couldn't stop eating. They started gaining weight at six weeks of age, and by the time they were ten weeks old, they were severely obese.'

Clinical trials on people are probably years away but Dr Matharu believes that CRISPR-A could provide 'a potential cure for certain forms of obesity as well as hundreds of other diseases'.

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