Physical things happen when the danger is imminent. Our heart rate and breathing speed up and we feel something run through our body as we discuss the decision to fight or run away.

It has long been thought that these physiological changes are caused, at least in part, by adrenaline, a well-known hormone – but it may not be all that.

Researchers led by Columbia University in the United States claim that studies suggest that a lesser-known hormone derived from bone, called osteocalcin, plays an important role.

As soon as the brain recognizes the danger, the skeleton asks the skeleton to flood the blood with osteocalcin, says lead researcher Gerard Karsenty, adding that "this completely changes the way we think about how responses to acute stress occur.

Karsenty and his colleagues have already shown that upon release of osteocalcin, it circulates in the blood to affect the functions of the biology of the pancreas, brain, muscles and other organs.

A series of studies conducted since then has shown that osteocalcin helps regulate metabolism by increasing the cells' ability to absorb glucose, improves memory, and helps animals run faster with greater endurance. .

In the new job, described in the journal Cell metabolism, the researchers presented mice with predator urine and other stressors and looked for changes in the bloodstream. Two to three minutes later, they saw their osteocalcin levels increase.

They found similar osteocalcin outbursts in people subjected to the stress of public speaking or cross-examination.

As osteocalcin levels increased, heart rate, body temperature, and blood glucose levels in mice also increased as the response to combat or flight became effective.

In contrast, genetically modified mice, unable to manufacture osteocalcin, or its receptor, were totally indifferent to the stressor.

"Without osteocalcin, they did not react strongly to the perceived danger," says Karsenty. "In the wild, they would have a short day."

In the final test, the researchers were able to elicit an acute stress response in unstressed mice, simply by injecting large amounts of osteocalcin.

They claim that their findings could also explain why animals without adrenal glands and insufficient adrenal patients – who have no way to produce adrenaline or other adrenal hormones – can develop an answer. of acute stress.

In mice, this ability disappeared when the mice were unable to produce large amounts of osteocalcin.

"This shows us that circulating levels of osteocalcin are enough to trigger the response to acute stress," says Karsenty.

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