"We are, in essence, temporarily converting mice from warm-blooded to cold-blooded creatures, which is exactly the same thing that happens naturally when mammals hibernate," said lead investigator Mark Roth, Ph.D., whose findings will be published in the April 22 issue of Science.
"We think this may be a latent ability that all mammals have -- potentially even humans -- and we're just harnessing it and turning it on and off, inducing a state of hibernation on demand," said Roth, a member of Fred Hutchinson's Basic Sciences Division.
During a hibernation-like state, cellular activity slows to a near standstill, which reduces dramatically an organism's need for oxygen. If such temporary metabolic inactivity ?and subsequent freedom from oxygen dependence ?could be replicated in humans, it could help buy time for critically ill patients on organ-transplant lists and in operating rooms, ERs and battlefields, Roth said.
"Manipulating this metabolic mechanism for clinical benefit potentially could revolutionize treatment for a host of human ills related to ischemia, or damage to living tissue from lack of oxygen," said Roth, also an affiliate professor of biochemistry at the University of Washington School of Medicine.
Collaborators on the research included first author Eric Blackstone, a graduate research assistant in Roth's laboratory and a member of the joint Fred Hutchinson/University of Washington Molecular and Cellular Biology Program; and co-author Mike Morrison, Ph.D., a staff scientist in Roth's lab.
Clinical applications of induced metabolic hibernation could include t