It seems as thought this obesity gene can be edited and defeated by a ground-breaking technique which would remove the problematic DNA coding, and substitute it with a better DNA sequence that would burn fat more efficiently.
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Obesity can lead to a number of medical conditions such as type 2 diabetes, cancer and cardiovascular disease. That result indicates that the white-to-beige fat switch works in fat tissue, not in the brain. “You now have a pathway for drugs that can make those fat cells work differently”.
In further experiments, they established that IRX3 and IRX5 control thermogenesis – a cell process for using energy stores to generate heat – in fat cells.
“Early studies of thermogenesis focused primarily on brown fat, which plays a major role in mice, but is virtually nonexistent in human adults. Instead they dissipated more energy, even in their sleep, suggesting a dramatic shift in their global metabolism”, said Dr. Claussnitzer, in the report by Discovery News.
“We could narrow down a genetic region spanning 47,000 nucleotides to reveal a single- nucleotide adjustment, and explain precisely how it leads to loss of repressor binding, activation of a regulatory region, gain of distal gene expression, a change in adipocyte metabolism, and ultimately obesity at the organism level”, explained Claussnitzer. In risk individuals, a thymine (T) is replaced by a cytosine (C) nucleobase, which disrupts repression of the control region and turns on IRX3 and IRX5. “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”.
About 40 percent of Europeans and 42 percent of Southeast Asians carry the obesity-risk variant, Kellis says. “But more importantly, the uncovered cellular circuits may allow us to dial a metabolic master switch for both risk and non-risk individuals, as a means to counter environmental, lifestyle, or genetic contributors to obesity”.
And genetic tinkering in mice and on human cells in the lab suggests this can be reversed.
Studies show, however, that this view largely ignores the genetic component of obesity, and that our metabolisms can be manipulated into burning fat cells quicker.
Then, they showed that they could manipulate this new pathway to reverse the signatures of obesity.
According to Professor Melina, the result of the study enables the possibility of “reprogramming” the fat stores in the body to be expended instead of being stored.
Researchers said they are now forming partnerships with academics and industry to explore therapeutic options – and perhaps a cure – for obesity. Until now, they didn’t know how it tied to appetite or other factors contributing to obesity.
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The highly-anticipated educational tracks for the 2015 R&D 100 Awards & Technology Conference feature 28 sessions, plus keynote speakers Dean Kamen and Oak Ridge National Laboratory Director Thom Mason.
