It turns out that body shaming over obesity is not just hurtful, it’s actually based on a lingering falsehood. Activists claiming that some people become overweight without eating more are right, new genetic research confirms. There is a genetic mutation that millions of Americans possess that causes some people to become obese without eating more than a person of average weight. This genetic mutation affects how calories are utilized. It was once an incredibly useful genetic mutation. Over the course of evolution, this mutation survived, because it helped humans survive during times of famine, researchers say.
Some people remain unconvinced by current social awareness campaigns that obesity can be fault-free. The new research published in the esteemed journal Proceedings of the National Academy of Sciences might finally change their minds.
The researchers designed a mouse study to examine a genetic mutation of the gene ankyrin-B. This mutation was suspected of causing obesity. Mice with mutations in this gene are more obese than mice that don’t have this genetic mutation. This gene is found in every tissue in the body. It was discovered a few decades ago by Dr. Vann Bennett, the senior author of the new study and professor of biochemistry at Duke University School of Medicine.
The link to obesity was first observed only a few years ago by a student working with Dr. Bennett named Jane Healey. Healey wanted to understand why mice with the mutated gene were fatter than their fellow mice. In order to study this, Healey made mice with the human variants of the ankyrin-B gene. These mice were very different from the mutation-free mice, according to Medical News Today. Instead of spreading calories to a variety of tissues to be used for energy, these mice stored most of their calories immediately in fat tissue.
Figuring out how the ankyrin-B gene worked was at the root of the new study though. Bennett worked with Damaris Lorenzo from the University of North Carolina at Chapel Hill to learn about the link between the gene mutation and obesity. In order to learn more, they turned off the gene entirely, according to Medical News Today. If mice with a mutated version of this gene became obese, what would happen if the gene was not functioning at all?
It turns out that the fat cells of mice without the gene functioning were twice as large, despite the fact that they were eating the same amount and exercising the same amount as the control mice. Plus, there was an increased accumulation of lipids that “spilled over” into other areas of the body too. Specifically, the lipids went on to affect the liver and muscles. This led to inflammation and the disruption of insulin.
Dr. Bennett explained that there was a “common belief in the field that much of obesity can be traced back to appetite and the appetite control centers that reside in the brain.” He added that this shows that there is actually such a thing as fault-free obesity. More than one percent of Caucasians and more than eight percent of African Americans carry a mutation on this gene.
Bennett said that in current times, ankyrin-B variants could be fueling the obesity epidemic. Future research will examine more about this gene and its impact on metabolism. They will also look into ways this information could help people figure out appropriate dietary needs based on their genetics.
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