Exercise is great for preventing obesity, but some of the excess weight that we carry is out of our control.
Obesity is not great for health, and there’s a lot that you can do to keep your weight in check. Diet, exercise, et cetera.
But just because there are some factors that you can control, it doesn’t mean that being overweight is your fault.
In fact, lifestyle changes only go so far and new research confirms it: a genetic mutation controls how much fat we store, and millions of us carry it.
What’s more, the gene in question may have evolved to keep us safe during times of famine. So, if we’re really keen on blaming someone, we can blame evolution — although we’re probably better off refraining from blame and judgement altogether.
If social awareness campaigns against the stigma attached to obesity haven’t managed to convince us yet, maybe this new study — published in the journal Proceedings of the National Academy of Sciences — will.
Which gene is to blame for obesity?
The new study was carried out in mice, but our fellow mammals offer a great window into how our own human bodies work.
Apparently, mice that have mutations in a gene called ankyrin-B are fatter than mice that don’t. Ankyrin-B can be found in every bodily tissue, tying proteins to the inside of a cell’s membrane.
The effect of this gene mutation was first noticed a few years ago by Jane Healey, a Ph.D. student working with Dr. Vann Bennett, the senior author of the new study. (As an interesting aside, the gene itself was first discovered more than 30 years ago by the same Dr. Bennett.)
To figure out why mice with this mutation were fatter than their fellow rodents, Healey “designed” mice that had human variants of the ankyrin-B gene.
Much to their surprise, the researchers saw that these mice grew fat — and fast! The rodents stored their calories in fat tissue, instead of spreading them to other tissues where they would be burned to create energy.
“The problem is,” explains Dr. Bennett, “we still didn’t know how this gene worked. There is this 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. But what if it isn’t all in our head?”
To find out, Dr. Bennett — together with Damaris Lorenzo, an assistant professor of cell biology and physiology at the University of North Carolina at Chapel Hill — embarked on the new study.
How a gene can lead to ‘fault-free obesity’
So, in the study, they completely knocked out the ankyrin-B gene in mice. The team repeated some of the previous experiments and found that the fat cells of the mice with this gene knocked out were twice as large.
This happened despite the fact that the mice were exercising and eating the same amount as the normal-weight ones.
“We quickly learned that the increased accumulation of lipids in fat cells ‘spilled over’ to the liver and muscles,” explains Prof. Lorenzo.
“The abnormal accumulation of fat in these tissues,” she adds, “led to inflammation and disruption of response to insulin, a hallmark of type 2 diabetes.” She goes on to say, “A similar cascade of events is what often takes place in humans, and that is why obesity can be so detrimental to our health.”
In fact, more experiments revealed that mutating or deleting the ankyrin-B gene altogether changes another protein, which basically opens the gates for blood sugar to enter fat cells.
“We found that mice can become obese without eating more, and that there is an underlying cellular mechanism to explain that weight gain […] This gene could enable us to identify at-risk individuals who should watch what kind of calories they eat and exercise more in order to keep their body weight under control.”
Dr. Vann Bennett
“We call it fault-free obesity,” says Dr. Bennett, who is also a professor of biochemistry at Duke University School of Medicine in Durham, NC.
“We believe this gene might have helped our ancestors store energy in times of famine,” he adds. “In current times, where food is plentiful, ankyrin-B variants could be fueling the obesity epidemic.”
According to the researchers, 1.3 percent of Caucasians and 8.4 percent of African Americans carry a mutation of this gene.
So, in the future, Dr. Bennett and his team plan to identify people with these genetic variants to see how they affect metabolism.