Scientists at the University of Utah are studying how bears and other mammals hibernate in search of genetic clues to the fight against obesity and related diseases in humans. By finding the right genetic “switch”, scientists may be able to understand why some animals are not affected by pathological obesity and related diseases.
Hibernation is an adaptation of many mammalian species to adverse environmental conditions in winter. By foraging in late autumn, these animals are able to build large enough fat reserves to stop their activities and enter their nests, and comfortably survive the cold winter. It’s a process that scientists are very interested in – not only because it’s an interesting puzzle, but also because of its medical potential or as a way to study astronauts sleeping on most long interstellar missions.
Another interesting fact is that hibernating animals seem to be resistant to all kinds of conditions. Before winter arrives, they eat a lot of food and increase their weight faster. But despite this, bears and other hibernating animals remain resistant to heart disease, cancer and diabetes and can remain dormant for months without losing bones or muscles. Scientists want to find out why and are looking for answers to DNA.
Dr Christopher Gregg, associate professor of neurology and anatomy, said: “Hibernating animals have developed a powerful ability to control their metabolism. Metabolism affects the risk of many different diseases, including obesity, type 2 diabetes, cancer and Alzheimer’s disease. We believe that understanding the genomic parts associated with hibernation will help us learn to control the risk of certain major diseases. One of the big surprises of our new study is that these important parts of the genome are hidden in 98% of the genome, which we used to call ‘junk DNA’. “
Gregg has teamed up with bioinformatics scientist Elliot Ferris to look for genetic “switches or regulatory elements” that give animals these abilities, hoping to identify similar areas in the human genome, especially those associated with obesity.
The team studied four species of hibernating mammals – 13-striped ground squirrels, light-shaven rat-eared bats, lemurs and Madagascar’s little hedgehogs – and found that each animal independently evolved short, uncoded DNA fragments called “parallel acceleration zones” and found similar areas near genes associated with human obesity more frequently than expected.
They found a special link to the genes of people with Prader-Willi syndrome, which leads to loss of appetite and morbid obesity. These genes have more “hibernation” acceleration zones than those that are not related to genetic diseases.
Hibernating animals produce similar appetite, but they may have evolved a genetic approach to turning the feature on and off, which could help researchers better understand and control obesity in humans. So far, the team has identified 364 potential genetic elements that may be associated with hibernation and obesity, and is currently testing mice using CRISPR epigenome editing techniques.
“Our results show that there is a ‘hibernating’ acceleration zone near genes associated with obesity,” Ferris said. So by aggregating data from humans and hibernating animals, we were able to find the main regulatory switches in the genome to control obesity in mammals. “
The study was published in Cell Reports.