Doctors get closer to throwing the genetic obesity switch

These processes were shown to operate without input from the brain – which means that in some cases, obesity is not just caused by bad habits.

Using human fat cells, the researchers found they could manipulate FTO in cells from individuals with the obesity-prone version to switch off IRX3 and IRX5, restore thermogenesis to non-risk levels and switch off genes that promote fat storage.

Now the researchers are hoping to get rid of obesity, a disorder that affects more than 500 million people worldwide and contributes to type 2 diabetes, cardiovascular disorders and cancer.

Researchers say it is not known how long it will take to develop an effective treatment but said it is unlikely there would ever be a pill that will let people eat whatever they like without gaining weight.

Researchers used a new technology called the Crispr/Cas9 system to edit the DNA code and fix the sequence in mice and human cells.

The scientists believe the injection could prevent or even cure obesity in those people with the faulty gene and negate the effects of a high-fat diet. They, subsequently, established a hyperlink from FTO to the management of whether or not fats cells burn or retailer fats, with out going by way of the mind.

The work was led by scientists at MIT and Harvard University and published online Wednesday by the New England Journal of Medicine. They predicted that the specific T-to-C single-nucleotide adjustment within FTO is responsible for the obesity association by repressing an evolutionarily-conserved gene regulator called ARID5B. With thermogenesis turned off, fat accumulates in the body and obesity sets in.

For his or her research, the group examined recognized gene management circuits from over 100 tissues and cell varieties. However, the role of genetics can not 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.

About 40 percent of Europeans and 42 percent of Southeast Asians carry the obesity-risk variant, Kellis says.

When researchers inhibited the corresponding gene in the fat cells of mice, the animals’ metabolism soared and they shed weight without eating less or exercising more. Disruption also resulted in a cell-autonomous developmental shift from energy-dissipating beige adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial thermogenesis and increase in lipid storage.

Kellis’s team now plans to see whether tinkering with the IRX genes can make obese mice lose weight. Instead, the variant doubles the activity of two genes, IRX3 and IRX5, which are involved in determining which kind of fat cells will be produced.

“Whether these findings will lead to new therapies for obesity is less certain”, Merkestein says, “because it’s likely the switch between beige and white fat cells is set during development of the embryo, and therefore it may already be too late to intervene in adulthood”.