Grizzly bears’ ability to hibernate for up to four months without discomfort may be key to helping prevent astronauts and medical patients from developing muscle atrophy, according to a new study. An international team led by Michael Gotthardt of the Max Delbruck Molecular Medicine Center (MDC) in Berlin is looking for genetic clues to learn more about the secrets of hibernating grizzly bears.
If a person tries to imitate a hibernating grizzly bear, if not fatal, the results can have a devastating effect on their health. When a bear goes to hibernate after eating food to increase body fat, it can hibernate for months and still wake up healthy in the spring. However, humans under similar conditions will suffer from blood circulation and psychological problems, as well as bone loss and muscle atrophy.
One of the reasons grizzly bears are so capable of doing so is because of their metabolism. As the heart rate drops and the animal becomes resistant to insulin, it stops excreting metabolic waste, reabsorbs amino acids from the urine, and blood nitrogen levels rise sharply. However, the way it keeps the muscles almost complete is of particular concern. To understand the mechanisms of muscle preservation, Gotthardt’s team tried to reveal genes in bears’ muscle cells that are transcribed and converted into proteins.
For the study, the team took samples from grizzly bears during hibernation. These were then compared with observations of elderly or bedridden human patients, mice and nematodes. Nematodes are particularly useful because their genes can be turned off relatively easily to see their effects on muscle growth, helping to narrow the range of candidate genes.
“By combining advanced sequencing techniques with mass spectrometry, we wanted to determine which genes and proteins were up or down during hibernation,” Gotthardt said. “One thing the team found was that non-essential amino acids (NEAAs) played an important role in changing the metabolism of bears and in preventing muscle atrophy.
“In experiments where isolated muscle cells in humans and mice show edatrophy, NEAAs can also stimulate cell growth,” Gotthardt said. But it has been known from earlier clinical studies that the application of amino acids in the form of pills or powders is not sufficient to prevent muscle atrophy in the elderly or bedridden. Obviously, it is important for the muscles themselves to produce these amino acids – otherwise, amino acids may not reach where they are needed. “
The team is currently studying a group of genes in mice that control circadian rhythms to better understand how what they learn edify effective therapies.
“We’re going to look at the role of inactivation of these genes,” Gotthardt said. After all, they are suitable for treatment only if the side effects are limited or there are no side effects at all. “
The study was published in the journal Scientific Reports.