In recent studies that could shift how we approach diabetes and neurodegenerative diseases, University of Utah Health scientists have identified a genetic link between hibernating mammals and humans that might unlock new treatment avenues. The research, published in Science, investigates hibernators' extraordinary ability to maintain physiological stability through extended periods without sustenance, a feat thought to be potentially replicable in human biology.
This groundbreaking work has uncovered that human DNA contains the same genetic structures, known specifically as the "fat mass and obesity (FTO) locus," that hibernators leverage to manage their incredible metabolic changes. Chris Gregg, a professor at the University of Utah Health and senior author on the studies, illuminated the significance of these genetic sections, remarking, "What's striking about this region is that it is the strongest genetic risk factor for human obesity," as per At The U. Gregg’s team believes that learning to similarly adjust these genes could help to dramatically enhance our metabolic flexibility and even, potentially, to help reverse type 2 diabetes after a return from a hibernation-like state.
The studies utilized various whole-genome technologies to zero in on the DNA regions most crucial for hibernation. They identified sequences unique to hibernating species, pinpointed genes that respond to fasting, and then focused on 'hub' genes central to these metabolic shifts. “If a region doesn’t change much from species to species for over 100 million years but then changes rapidly and dramatically in two hibernating mammals, then we think it points us to something that is important for hibernation, specifically,” bioinformatician Elliott Ferris told At The U.
The implications of these findings are robust, offering hope for treatment breakthroughs in age-related diseases. The scientists have found that many of the genomic elements associated with hibernation tend to disrupt, rather than enhance, specific DNA functions. This suggests that our metabolic 'thermostat' may be unnecessarily limited. "If we could regulate our genes a bit more like hibernators, maybe we could overcome type 2 diabetes the same way that a hibernator returns from hibernation back to a normal metabolic state," said Ferris, as obtained by At The U. This deep dive into our genetic code could ultimately awaken dormant human capacities akin to those of hibernators.
