In a new study, researchers found that a molecular “trick” that kept our ancient ancestors from starving may now be contributing to the obesity epidemic.
The research was conducted by a team from NYU School of Medicine.
In starvation times, animals were more likely to survive if they could hoard and stretch out their stored energy.
Even if an animal secured a rare feast, evolution smiled on the storage of excess fuel as fat, given the likelihood of a quick return to starvation.
In the new study, the team found that an anti-starvation mechanism that has become a curse in times of plenty because it sees cellular stress created by overeating as similar to stress created by starvation.
This can put the brakes on our ability to burn fat.
The researchers found that the natural function of a protein called RAGE on the surface of fat cells is to stop the breakdown of stored fat in stress.
This finding may partly explain why 70% of American adults are overweight or obese.
According to the team, the most efficient way for evolution to create an anti-starvation mechanism was from ancient systems that helped animals use food for cellular energy and recover from injury.
Also wired into these primal mechanisms was the hormone adrenalin, which signals for the conversion of fat into energy as animals run from predators, or into body heat when they get cold.
This convergence means that RAGE may block “fat-burning” called for when people starve, freeze, get injured, panic, or ironically, overeat.
The team found that removing RAGE from fat cells caused mice to gain up to 75% less weight during three months of high-fat feeding compared with mice that had the RAGE brake on.
In addition, transplanting fatty tissue lacking RAGE into normal mice also decreased weight gain as they were fed a high-fat diet.
The team hopes the new finding can help develop new methods to help keep bariatric surgery patients, and patients undergoing medical weight loss regimens, from regaining lost weight.
The lead author of the study is Ann Marie Schmidt, MD, the Dr. Iven Young Professor of Endocrinology at NYU School of Medicine.
The study is published in Cell Report.
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