Scientists have discovered that genes linked to hibernation in animals are also present in humans — and they could offer surprising medical advantages. A new pair of studies suggests that unlocking the power of these genes might one day help treat conditions like obesity, diabetes, and even brain injuries.
Researchers at the University of Utah, led by genetics professor Christopher Gregg, explored how certain mammals adjust their metabolism during hibernation. Their findings, published in the journal Science, point to a shared genetic toolkit that humans may be able to access.
What the Research Found
Hibernating animals, such as ground squirrels, have unique metabolic traits. For instance, they can temporarily develop insulin resistance to help gain weight before winter — and then reverse it when they begin hibernating. They also have built-in protection against brain damage from sudden changes in blood flow, something that would typically cause strokes in humans.
Gregg and his team believe these biological “superpowers” could be harnessed in humans if we better understand how these genes work.
“We have these genes in our DNA,” Gregg explained. “It’s a matter of learning how to switch them on and off in the right way.”
Studying Mice for Clues
To test their theory, the researchers used mice — which don’t hibernate but can enter a brief torpor-like state when fasting. Using CRISPR gene editing, the team deactivated specific DNA switches near a gene cluster known as the FTO locus. This gene region is already linked to metabolism, weight gain, and obesity in humans.
The scientists “knocked out” five of these switches — called conserved noncoding cis elements (CREs) — to see how the mice reacted. The results were striking: some mice gained more weight, others burned energy faster, and some even changed their food-seeking behavior.
One particular DNA switch, called E1, caused female mice to gain significantly more weight on a high-fat diet. Another, E3, changed how mice searched for food.
Why It Matters for Humans
These findings are especially exciting because the FTO locus exists in both animals and humans, suggesting the mechanisms could be similar.
“This is a very promising development,” said Kelly Drew, a hibernation biology expert at the University of Alaska Fairbanks. “The genes are part of a metabolic toolkit that may one day be used to improve human health.”
However, the research is still in early stages. Scientists caution that simply copying genetic changes from mice to humans won’t be straightforward. Unlike mice, humans can’t enter torpor on their own, and real hibernation is triggered by seasonal and hormonal signals, not just fasting.
Joanna Kelley, a genomics professor at UC Santa Cruz, added that future research should look at other animals that don’t experience torpor and explore the full impact of tweaking these genes.
What’s Next?
Gregg’s team is now planning to test what happens when multiple hibernation-linked gene switches are altered at the same time. They also aim to explore sex-based differences, after noticing that some effects varied between male and female mice.
Eventually, Gregg believes it might be possible to develop drugs that mimic the benefits of hibernation-related gene activity — such as protecting the brain or regulating metabolism — without putting people into actual hibernation.
“This could open new doors in treating metabolic diseases and neurological conditions,” Gregg said.
A Step Toward Human ‘Superpowers’?
While we’re still far from humans entering a hibernation-like state, this research offers an intriguing glimpse into what might be possible with the right genetic insights. It also highlights how ancient evolutionary traits, once thought to be dormant, could hold the key to solving modern health problems.
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