University of Utah: Understanding Hibernation Mechanisms Could Help Overcome Obesity

Why are obese people more likely to develop diabetes, inflammation or even cancer and not huge mammals like bears? To try to understand this, U.S. researchers have analyzed the mechanism of hibernation. According to their study published in Cell Reports, hibernating animals have developed advanced mechanisms that allow them to automatically stop the activity of certain genes associated with obesity.

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Sleeping Bear

Sleeping Bear

In the fall, many mammals gain weight and become resistant to insulin. Then, to survive the winter, when food is scarce and nature becomes more hostile, they go into hibernation: they fall asleep, body temperature decreases, the heart beats more slowly, breathing slows down, as well as other metabolic processes. When winter is over, the hibernator can easily lose excess weight and his body will automatically reverse insulin resistance. For Elliott Ferris and Christopher Gregg, researchers at the University of Utah in Salt Lake City, this control of obesity may be due to certain genetic mechanisms involved in regulating hibernation.

To test their hypotheses, the scientists decided to analyze the genomes of four species of hibernating mammals: the thirteen-lined ground squirrel, the small brown bat, the gray mouse lemur, and the lesser hedgehog tenrec. When comparing them, they observed that they had developed a series of short DNA sections called parallel accelerated regions.

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Mice appear to have similar obesity-related genes to humans. To confirm this relationship, the researchers analyzed a set of genes that cause Prader-Willi syndrome, a rare genetic disease in humans. One of the characteristics of this disease is excess appetite, which can lead to obesity. They later discovered that these genes were associated with a greater number of regions accelerated by hibernation than those that had nothing to do with this genetic condition. Therefore, hibernating animals may have developed advanced mechanisms to automatically stop the activity of certain genes associated with obesity.

Researchers have also identified up to 364 genetic elements that can help regulate hibernation and control obesity. Using specialized gene-editing technology, scientists are now testing the role of these 364 genetic elements in mice.

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“Hibernators have evolved an incredible ability to control their metabolism,” says Christopher Gregg, Ph.D., associate professor in the Department of Neurology & Anatomy at Utah University. He added that metabolism determines the risks of many diseases, including obesity, type 2 diabetes, cancer, and Alzheimer’s disease. He believes that understanding the parts of the genome that are linked to hibernation will help control the risks of some of these important diseases.  Also, a big surprise in the new study is that these important parts of the genome have been hidden from us in 98% of the genome that does not contain genes an area labeled as junk DNA. He concluded that since obesity and metabolism determine the risks of so many different diseases, the discovery of these parts of the genome is a truly exciting discovery that sets the stage for many important new directions of research. And as a result, we have new projects dealing with aging, dementia and metabolic syndrome.

Today, obesity is a public health problem. It is associated with an increased risk of cardiovascular, cervical, ovarian and breast cancer in women, prostate cancer in men, colon and gallbladder cancer in both sexes. In addition, people with obesity are more likely to have diabetes, liver, kidney, or respiratory problems, high blood pressure, headaches, stomach pain, fatigue, urinary incontinence, excessive sweating, menstrual disorders and polycystic ovaries in women.

Therefore, every year in the world, obesity causes at least 2.8 million deaths. In the OECD, the average number of obese people is 19.5%. The United States, Mexico, New Zealand, and Hungary are the most affected.

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References

https://www.eurekalert.org/pub_releases/2019-11/uouh-hma112119.php

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