From Our 2014 Archives
The 'Bear' Facts on Obesity and Diabetes
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However, unlike people, insulin levels in grizzly bears do not change, the researchers found. Instead, the bears' cells seem to be able to control their ability to respond to insulin.
In fact, in the fall -- when grizzly bears are most obese -- they are also the most sensitive to insulin, says a team led by Dr. Kevin Corbit, of the drug maker Amgen, Inc.
According to Corbit's group, this happens because the activity of a key protein found in fat cells, called PTEN, is shut down.
In fact, weeks into hibernation, grizzly bears develop a "natural" state of diabetes that is cured when they wake up in the spring, according to the study, which is published Aug. 5 in the journal Cell Metabolism.
During hibernation, grizzly bears also store the fuel their bodies need to survive the winter in fat tissue. In other obese animals however, fat builds up in the liver and muscles, Corbit's team pointed out.
The bear findings are "in contrast to the common notion that obesity leads to diabetes in humans," Corbit said in a journal news release. In fact, the finding suggests that obesity and diabetes "may exist naturally on opposite ends of the metabolic spectrum," he said.
Corbit stressed that these findings have yet to be borne out in humans. However, "we believe that these and other data do support a more comprehensive and perhaps holistic approach to caring for patients with diabetes and/or obesity," he said.
His team believes that the mechanisms that lead to obesity in some people -- such as lower levels of PTEN -- might also protect them from diabetes. On the other hand, what leads other people to develop diabetes might also protect them from becoming obese.
"This more sophisticated understanding of the relationship between diabetes and obesity should enable researchers not only to develop therapies targeting these mechanisms, but also to identify the appropriate patients to whom these therapies should be targeted," Corbit said.
-- Mary Elizabeth Dallas
SOURCE: Cell Press, news release, Aug. 5, 2014