Genetic traits linked to hibernation in animals might hold dormant capabilities in humans, according to scientific research.
New Study Sheds Light on Hibernation Genes and Their Potential Impact on Human Health
A groundbreaking study has revealed significant insights into the genetic controls driving hibernation in animals, potentially paving the way for new treatments for medical conditions such as type 2 diabetes and insulin resistance.
The research, conducted on mice, focused on certain conserved noncoding cis elements (CREs) that were found to be near a gene cluster called the "fat mass and obesity-related locus," or the FTO locus, which is also present in humans.
By using the gene-editing technique CRISPR to deactivate these CREs, the researchers were able to change the mice's weights, metabolic rates, and foraging behaviors. For instance, knocking out CRE E1 in female mice caused them to gain more weight on a high-fat diet, while deleting CRE E3 altered the foraging behavior of both male and female mice.
The study's lead author, Drew, points out that torpor in mice is triggered by fasting, while true hibernation is triggered by hormonal and seasonal changes and internal clocks. However, the findings could still be relevant to humans, as the underlying genes don't differ much between mammals.
One key discovery of the study is the role of the FTO locus, a known strong genetic risk factor for obesity in humans, in hibernation-related metabolic regulation. In hibernators, these regions are used differently to control metabolism and energy use, suggesting potential targets for human metabolic disease therapies.
Gregg, another researcher involved in the study, believes it could be possible to tweak the activity of humans' "hibernation hub genes" with drugs, potentially providing benefits without requiring hibernation. Beyond metabolic conditions, hibernation genes also help protect animal brains from damage due to blood flow changes and may prevent muscle atrophy and nerve degeneration, indicating broader therapeutic potential for neurodegenerative diseases alongside diabetes treatment.
One of the key findings of the study is the reversible insulin resistance observed in hibernating mammals, such as ground squirrels. Understanding how they switch this on and off could help treat the persistent insulin resistance that defines type 2 diabetes in humans. The study also highlights the potential for gene variants within the FTO locus to elevate the risk of obesity and related conditions.
While much remains unknown about why the effects of some deletions differ between genders or how changes in foraging behavior in mice might manifest in humans, the study points the field in a new direction in terms of understanding the genetic controls driving changes in hibernators. The hope is that by studying how hibernation-related genes adjust metabolism and insulin sensitivity in animals and identifying analogous gene regulatory regions in humans, scientists can develop new treatments that could reverse or mitigate type 2 diabetes and insulin resistance, closely mimicking the natural "superpowers" of hibernation.
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- This study's identified role of the FTO locus in hibernation-related metabolic regulation, a known genetic risk factor for obesity in humans, offers promising insights for developing new treatments for chronic diseases like type 2 diabetes and insulin resistance, which are categorized under the broad umbrella of health and wellness.
- Beyond the potential for treating type 2 diabetes, understanding how hibernating mammals exhibit reversible insulin resistance and how their hibernation genes protect their brains from damage also presents therapeutic possibilities for neurodegenerative diseases, extending its relevance to a wide range of medical conditions.
