Researchers studying portly grizzly bears have discovered a natural state of diabetes that serves a real biological purpose -- and it’s reversible. According to a new study published in Cell Metabolism, the bears are obese in the fall, become temporarily diabetic during hibernation, and somehow they’re “cured” by the time they wake up in the spring. 

Animals routinely cope with conditions that would cause diseases in humans. In bears and people alike, the hormone insulin helps carry sugar in the blood to cells around the body. Patients with type 2 diabetes produce insulin, but their cells don’t respond to it -- called “insulin resistance.” The pancreas reacts by producing more insulin, but over time the system stops making enough when blood sugar levels spike. The confluence of diabetes and obesity is a worldwide epidemic. 

Some scientists have turned to natural extreme biology: Hibernating animals become obese annually to survive long periods of food scarcity. Despite their striking increases in body weight and fat in preparation, they don’t suffer from metabolic disorders. “I believe there is an animal out there that has the answer to any human ailment,” Kevin Corbit of California-biotech Amgen tells Nature. 

So, Corbit and colleagues studied grizzly bears (Ursos arctos horribilis) housed in a colony in Washington state. They monitored the bears in October (pre-hibernation gluttony), January (hibernation), and May (post-hibernation awakening) -- collecting blood and tissue samples, recording body weight, and measuring percent body fat.

They found that, unlike in humans, insulin and blood sugar levels in grizzly blood did not change. These levels stayed remarkably constant. Turns out, the cells that communicate with insulin can turn their ability to respond to the sugar-regulating hormone on and off, like a dimmer.

When grizzlies are the most obese, they’re also the most “insulin sensitive” -- or least diabetic. They become this way by shutting down the activity of a protein called PTEN in the autumn, but only in their fat cells. That way, the bears' cells keep responding to insulin, and signals to store sugar, even as they pack on the pounds. Grizzlies end up storing all the fuel they'll need for wintertime in their fat tissue -- and not in their liver and muscle, which are common places for fat to accumulate in people and other animals with obesity.

This state of “augmented insulin sensitivity while obese” happens just before the insulin resistance (or temporary diabetes) that they experience during hibernation -- which keeps enough sugar in their blood for them to survive. By spring, they became sensitive to insulin again. You can see the cycle in this graphical abstract.

"This is in contrast to the common notion that obesity leads to diabetes in humans," Corbit explains in a news release. “Our results clearly and convincingly add to an emerging paradigm where diabetes and obesity -- in contrast to the prevailing notion that the two always go hand-in-hand -- may exist naturally on opposite ends of the metabolic spectrum.”

If shutting off PTEN helps obese bears maintain insulin sensitivity, Corbit tells Science, turning off the pathway in overweight people could prevent or treat diabetes.

Images: shutterstock.com (top), Kevin Corbit (middle)