Cure Obesity With One Injection? Scientists Claim to Have Found a Solution

The key gene connected to obesity, responsible for people getting fatter, has finally been figured out. Thermogenesis can be triggered from exercise, a proper diet, or by spending time in cold weather.

“It’s a big deal”, said Dr. Clifford Rosen, a scientist at Maine Medical Center Research Institute and an associate editor at the medical journal. Fat tissue cells have been withdrawn from human respondents and the gene has been deactivated to see the triggering results. Some 44 per cent of Europeans carry a variant that raises their risk of obesity by around 30 per cent, increasing body weight by about 3 kilograms. Those genes, in turn, were preventing fat from being burnt through a process known as thermogenesis-where fat cells get rid of energy in the form of heat, instead of storing it as fat-that happens naturally in those with healthy FTO gene regions. “Our results indicate that the obesity-associated region acts primarily in adipocyte progenitor cells in a brain-independent way”.

Scientists who analyzed the cell-level circuits surrounding the activity of the FTO gene – the one most strongly associated with obesity – have discovered a metabolic pathway that appears to exert overall control over whether our fat cells store or burn calories. By studying cells from people with mutations in an obesity gene called FTO, Kellis found that their cells contained certain mutations that inhibited the formation of beige fat. “We found a strong difference for both IRX3 and IRX5 in preadipocytes, revealing the target genes, cell type and developmental stage where the genetic variant acts, thus enabling us to begin dissecting its mechanism of action”.

The test has been conducted on a large group of lab mice and presupposed the blocking of the faulty gene in half of the respondents.

“By manipulating this new pathway, we could switch between energy storage and energy dissipation programs at both the cellular and the organismal level, providing new hope for a cure against obesity,” Kellis says.

In normal-weight mice, Kellis says, the effects of turning that knob are dramatic: “By changing the expression of one gene in these mice, they lose 50 percent of their body weight”.

Mice who had been bred to obese saw a reduction of body weight and all major fat stores, and complete resistance to a high-fat diet.

They also burned more energy even when asleep.

The New England Journal study may add still more impetus to exercise, because earlier research suggests that exercise may help turn white fat into brown or beige fat, Apovian says. “This can serve as a model for understanding the mechanistic basis of other non-coding variants in other diseases and traits”. But researchers might use similar strategies to those in this study to figure out how genetic variants are linked to other diseases. In primary adipocytes, knockdown of IRX3 or IRX5 restored thermogenesis in participants with the risk allele. 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.