Every autumn, the bears prepare for winter by stuffing themselves with food and becoming obese.
Weeks later during hibernation they enter a state similar to type 2 diabetes, only to "cure" themselves when they wake up in the spring.
US scientists studying the bears made the surprising discovery that when grizzlies are at their fattest they are also most sensitive to the blood sugar regulating hormone insulin.
This was achieved by shutting down the activity of a protein called PTEN in fat cells.
The finding is relevant to humans because obesity is strongly associated with type 2 diabetes.
Also, in contrast to humans, blood insulin levels in diabetic grizzlies did not change. Instead, cells that the hormone communicates with turned their response off and back on again when it was time to stop hibernating.
Lead scientist Dr Kevin Corbit, from the US biotech company Amgen Inc, said: "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.
"While care must be taken in extrapolating preclinical findings to the care of particular patients, 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."
Cellular mechanisms leading to obesity may in fact protect certain patients from diabetes, said Dr Corbit.
In other patients, mechanisms leading to diabetes may protect against obesity.
Humans with low levels of PTEN were likely to possess the bear-like quality of remaining highly insulin-sensitive even if obese.
"Moving forward, 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," Dr Corbit added.
The research is published in the journal Cell Metabolism.