How do bears manage to make the form of diabetes that they develop during their hibernation disappear in the spring? American researchers think they are one step closer to the answer.
People with diabetes have too much glucose, a form of sugar, in their blood. In the long term, this can lead to cardiovascular disease, among other things. The hormone insulin plays an important role in the condition. This substance removes glucose – which enters our body through food – from the blood and transfers it to body cells, where it serves as an energy source. Diabetes occurs when this happens too little. This is possible because the body does not produce enough insulin (type 1 diabetes) or because it becomes less sensitive, or resistant, to it (type 2).
By far the majority of people with diabetes have the second variant. Worldwide, more than a million people die each year, while the number of sick people is only increasing. It is not without reason that scientists are eagerly looking for new or improved treatments. A team of researchers from Washington State University in the United States hopes to find inspiration in nature. With bears, that is.
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The reason: bears develop a similar resistance to insulin during hibernation. This does not make the animals sick, but allows them to survive for months without food and water. When they eat again after waking up in the spring and the concentration of glucose in the blood increases, insulin sensitivity returns. A handy trick that may also restore sensitivity to insulin in humans, the researchers reason.
Disturbed hibernation
For that, it is necessary to understand exactly how the ‘on/off switch’ for insulin resistance functions in bears. To come up with an answer, the team subjected six grizzly bears, who live captive in a university research center, to an experiment. Fat tissue and blood samples were taken from each animal during the ‘active’ season as well as during hibernation. The researchers did the same while disrupting the bears’ hibernation by regularly feeding them a sugary drink for two weeks.
They then combined the different samples in the lab. This caused the necessary changes in the tissue, according to the research results published this week. Blood serum from the disrupted hibernation in particular had a major effect on cultured cells from adipose tissue taken during ‘normal’ hibernation. These began to exhibit behavior similar to that of active-season cells.
Translate to humans
Remarkably, only a few proteins were responsible for all the changes, the researchers concluded after an analysis. “There appear to be eight proteins that either independently or together regulate insulin resistance in hibernating bears,” said evolutionary geneticist Joanna Kelley, who contributed to the study.
These are proteins of which humans possess so-called homologues, she notes. In other words, for every protein there is a human counterpart, which descends from a common ancestor. “That means there may be a direct possibility of translation to humans.”
That is why the team is focusing on more research into the precise role of the proteins in turning insulin resistance on and off. In this way they hope to discover possible treatments for human diabetes. Whether the latter will actually happen remains to be seen, says Cees Tack, professor of medicine at Radboud University. Tack, whose own research focuses on treating diabetes in humans, doubts whether the cause of all the changes can be traced back to eight proteins. “The samples the team is studying come from only a small number of bears. That is very limited to come to firm conclusions.’
Moreover, the road to possible applications in humans is very long, says Tack. ‘It is possible that these eight proteins play an important role, but how they do this is still completely unknown. In fact, we don’t even know the exact function of most of them in the body. A great deal of further research is needed to map this out. After which it is still questionable to what extent this can teach us something about processes in the human body.’