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American researchers have found special genes in hibernating animals that regulate their metabolism and reduce energy consumption.
According to scientists, humans actually share the same DNA and genes associated with hibernation. Previous studies have shown that the use of this DNA can help treat many diseases.
“Hibernation gives us a number of different biometrically important superpowers”, — says senior author of the study, Professor of Human Genetics at the University of Utah, Christopher Gregg.
For example, gerbils can develop reversible insulin resistance, which helps them gain weight rapidly before hibernation, which then decreases once it begins. According to Christopher Gregg, a deeper understanding of how hibernating animals switch this mechanism could be useful in combating insulin resistance in the treatment of type 2 diabetes. Animals that hibernate protect their nervous system from damage that can be provoked by sudden changes in blood flow.
“When they come out of hibernation, their brains are filled with blood again. This often leads to serious consequences, such as stroke, but they have developed ways to prevent such injuries”, — says Christopher Gregg.
According to Christopher Gregg and his colleagues, harnessing genes associated with hibernation could provide humans with similar benefits. Based on the results of two studies, Gregg and his team found key mechanisms genes, that control genes associated with hibernation. They showed, how these genes differ in hibernating animals compared to non-hibernating animals.
In a series of laboratory experiments, the researchers also studied the effects of deleting these genes in mice. Although mice do not hibernate, they can enter a certain lethargic state with reduced metabolism, mobility, and body temperature. This state usually lasts no more than a day and after fasting for at least 6 hours.
Using the CRISPR gene editing technology, scientists have created mice with the is one of five conserved non-coding cis-elements (CREs) deactivated, that act like control levers for genes that encode proteins that perform biological functions. The CREs, that were the subject of the study, are located near a cluster of genes called the “fat mass and obesity-related locus” or FTO locus, which is also found in humans.
Gene variants found in this cluster are associated with an increased risk of obesity and related conditions. It is generally known that the FTO locus is important for the regulation of metabolism, energy expenditure, and body weight.
By activating CRE, the researchers were able to change the weight of mice, their metabolic rate, and their eating behavior. Some Deletions — structural mutations in which a part of a chromosome or DNA sequence is deleted, accelerated or slowed weight gain, others accelerated or slowed metabolism, and some affected the rate of recovery of body temperature in rodents after a lethargic state.
Deletion of one CRE, called E1, in female mice caused them to gain more weight on a high-fat diet than a control group with fully intact DNA. Deletion of another CRE, called E3, changed the males’ foraging behavior.
“This suggests that there may be important differences between hibernating and non-hibernating animals in their food search and decision-making processes, and the elements we have identified may be involved”, — explains Professor Christopher Gregg.
The authors of the study argue, that the findings may be relevant to humans, as human basic genes are not much different from animal genes. Christopher Gregg notes, that it is the way animals activate and deactivate these genes at different times and for different durations, in different combinations, forms different types.
According to professor, specializing in functional genomics at the University of California, Santa Cruz, Joanna Kelly, future studies should include animals that do not hibernate. Researchers will need to focus on all the effects of the removed CREs.
Specialist in hibernation biology at the University of Alaska Fairbanks Kelly Drew also notes, that stupor in mice is caused by starvation, while true hibernation is regulated by hormonal and seasonal changes, as well as the internal clock. Thus, while CRE and the genes identified in the study are likely critical components of the metabolic “toolkit” that responds to fasting, they may not be the “master switch” that turns deep sleep on or off.
According to Christopher Gregg, many questions remain. For example, why the effects of some deletions differ in female and male mice, and how changes in food-seeking behavior observed in mice may manifest themselves in humans.
The team also plans to investigate what happens if more than one CRE associated with deep sleep is removed from a mouse at the same time. Gregg believes that in the future it will be possible to use drugs to influence the activity of genes responsible for deep sleep in humans. The idea is that this approach will allow to use the benefits of the activity of these genes, such as neuroprotection, without the need for patients to fall into deep sleep.
The results of the study are published in the journal Science
Source: LiveScience
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