Bears are famous for many things. Eating honey. Being viscous and cuddly. Hibernating for months on end.
It’s this period of sustained rest that most interests German scientist Michael Gotthardt. The head of Neuromuscular and Cardiovascular Cell Biology at the Max Delbruck Center for Molecular Medicine (MDC) is convinced that studying what happens to bears’ muscles during hibernation — or, more accurately, what doesn’t happen to them — can help us prevent patients in hospitals from seeing their muscles waste away.
Bear genes
A post on the MDC site summarising a recent piece of research by Gotthardt and his team explains that bears go into hibernation at some point between November and January, during which time their heart rate and metabolism drop rapidly. They excrete “neither urine nor feces,” then wake up in the Spring, more or less ready to go about their everyday life.
A human, by contrast, would be incapable of surviving the period in a healthy way. The muscles of someone bedridden for months on end (or someone with an arm or a leg in a cast) would be much, much weaker, through a process known as atrophy. There are also blood clots and even psychological changes to contend with.
Gotthardt’s team has therefore been using “cutting edge sequencing techniques” and “mass spectrometry” to analyse bears’ muscle samples before and during hibernation.
“We wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation,” Gotthardt told the MDC site.
“This task proved to be tricky – because neither the full genome nor the proteome, i.e., the totality of all proteins of the grizzly bear, were known.”
It turns out that the bear cells contain proteins that “strongly influence” amino acid metabolism during hibernation, leading to higher amounts of protective, non-essential amino acids.
Further tests
The team then began working out how to apply the findings to humans. Previous tests have shown that simply giving older or sick people amino acid pills and powders is not enough — and that instead, the muscles themselves need to be induced to produce the acids.
Gotthardt therefore ran tests on atrophied muscle samples from mice, humans and worms to identify and narrow down the relevant genes. The MDC site reports that they found “a handful,” including the genes “Pdk4,” “Rora” and “Serpinf1.” Rora is of particular interest, as it is involved in the development of circadian rhythms — a natural, internal process that regulates the sleep-wake cycle and repeats roughly every 24 hours.
“We will now examine the effects of deactivating these genes,” Gotthardt adds. “After all, they are only suitable as therapeutic targets if there are either limited side effects or none at all.”
