Humans carry hidden hibernation genes that could treat diseases

Hibernating animals stretch the limits of biology, surviving for months without food or water. Their muscles stay strong, their body temperature drops to near freezing, and their brain and metabolism slow dramatically.

Despite these changes, the animals emerge healthy. They recover from conditions that resemble human diseases like Alzheimer’s, stroke, or diabetes.

Now, researchers think we might carry this resilience too. Studies published in the journal Science suggest that the genes powering hibernation might exist in human DNA. These genetic traits, once thought unique to hibernators, may lie dormant within us.

Understanding and unlocking these genes could lead to treatments for metabolic and neurodegenerative diseases.

How hibernators use special genes

Scientists focused on a gene cluster called the fat mass and obesity-associated (FTO) locus. Hibernating animals use it to control fat storage and energy during winter.

“What’s striking about this region is that it is the strongest genetic risk factor for human obesity,” said Dr. Chris Gregg from the University of Utah (U of U).

The team found nearby DNA regions that hibernators use to switch the activity of genes on or off. These controls don’t change the genes themselves. Instead, they regulate gene behavior, like adjusting volume in an orchestra.

These non-coding regions help hibernators gain weight before winter and burn fat efficiently while asleep.

Researchers inserted these DNA regions into mice. The results were clear. Some mice gained or lost weight depending on diet. Others had changes in body temperature recovery or overall metabolism.

“When you knock out one of these elements – this one tiny, seemingly insignificant DNA region – the activity of hundreds of genes changes,” explained Susan Steinwand, a scientist at U of U Health.

Hibernation genes control fat and energy

These DNA regulators don’t create new genes. Instead, they remove blocks that limit flexibility in metabolism. Hibernators may have evolved to lose certain constraints. That allows them to shift between active and dormant states easily.

“If we could regulate our genes a bit more like hibernators, maybe we could overcome type 2 diabetes the same way that a hibernator returns from hibernation back to a normal metabolic state,” said Elliott Ferris, MS.

The key difference between us and hibernators may be in how we regulate the same set of genes. This insight raises the possibility that humans could someday adjust their metabolism in similar ways.

Hibernation changed genes over time

To find these genetic clues, researchers used several advanced methods. They first searched for DNA regions that remained stable across most mammals for over 100 million years but showed recent and dramatic changes in hibernating species.

Such sudden shifts in long-conserved DNA strongly suggest adaptations specific to hibernation behavior.

Next, the researchers studied fasting mice. Fasting mirrors certain biological conditions seen in hibernation, including reduced energy intake and slowed metabolism. It triggers a complex cascade of gene activity.

The team tracked which genes turned on or off during this period and identified “hub” genes that regulate broader gene networks.

Interestingly, many altered regions in hibernators were located near these hub genes. These overlaps imply that evolutionary changes may have modified gene control switches to support hibernation.

The switches appear crucial for the coordination of metabolic and neurological functions. Scientists now consider these regulatory elements key targets for future genetic and medical research.

How this could help humans

Rather than inventing new traits, evolution in hibernators may have broken metabolic locks. Humans still have those locks in place. But our genes hold the same basic tools.

“Humans already have the genetic framework,” said Steinwand. “We just need to identify the control switches for these hibernator traits.”

The findings hint at future medical possibilities. If we identify and harness these regulatory switches, we may help humans survive extreme metabolic stress, reverse age-related decline, or treat chronic disease.

“There’s potentially an opportunity – by understanding these hibernation-linked mechanisms in the genome – to find strategies to intervene and help with age-related diseases,” noted Dr. Gregg.

“If that’s hidden in the genome that we’ve already got, we could learn from hibernators to improve our own health.”

The study is published in the journal Science.

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