They came to America with the first European settlers. Alongside us, they colonized the New World with the same hopes and dreams: to start a new life. All in all, they are not so different from us: they build homes (although sometimes they room with us), they have families (usually very large ones), they are pretty darn good at mazes, and they like cheese. In fact, we share 90% of the same DNA. They are like family to us…little, furry, plague-spreading brothers and sisters. But now they need our help. Millions of these beloved creatures are suffering as a result of a terrible crisis. Of course, I am referring to the global issue of mouse obesity.
While this debilitating condition may seem insurmountable at first glance, medical researchers from Tufts University and Yale University think they may have found a solution for our hairy brethren. This team of scientists recently discovered the FAT10 gene. According to Dr. Martin S. Obin, an adjunct scientist in the Functional Genomics Core Unit at Tufts University, “No one really knew what the FAT10 gene did, other than it was ‘turned on’ by inflammation and that it seemed to be increased in gynecological and gastrointestinal cancers.” Nevertheless, this gene can be found in all mammals, so they conducted an experiment to see what would happen if mice were engineered to lack this gene (Scutti, 2014).
Upon analysis to their ordinary control counterparts, the mutated mice simply couldn’t get fat. Even though they ate more food than the normal mice without the FAT10 gene, they had 50% less fat tissue. In addition, by eliminating the FAT10 gene, insulin levels in the mice were reduced, resulting in protection against diabetes and an increase in lifespan by 20%. As Dr. Obin noted, “Turning off the FAT10 gene produces a variety of beneficial effects in the mice, including reduced body fat, which slows down aging” (Scutti, 2014)
While the results from this experiment appear conclusive, scientists still don’t understand how the FAT10 gene works and how individuals will adapt to “dietary challenges” without this gene. For instance, they worry that, by eliminating the FAT10 gene, mice will have a harder time fighting off infections without the energy that is stored as fat. Currently, the genetically modified mice live in a sterile laboratory environment where the possibility of infections is reduced.
And that’s not all. The FAT10 gene isn’t the only gene associated with energy storage. Your body hosts a plethora of various “fat genes,” each playing specific roles in your metabolism. Scientists are still unraveling the DNA to exactly understand what the role of each gene plays in your body, but as Dr. Parks, a post-doctoral researcher from the Geffen School of Medicine at UCLA says, “If we understand how genetic factors influence so much of the population to become obese, we could potentially reverse it with more research” (University of Colorado Denver, 2013).
By finding the right combination of activated and deactivated fat genes, scientists may one day be able to reverse the process of obesity, potentially saving our furry relatives everywhere from their gluttony and help them lead longer, happier, healthier lives. However, there’s much research still to be done before that dream can become a reality. But never fear, there are already experimental drugs undergoing human trials as we speak. Within a few more years, they may be ready to be safely administered to mice. Until that time, however, only YOU can stop mouse obesity. So don’t just sit idle while your friendly neighborhood mouse becomes fat on the food you left lying around your dorm floor. Take action! And clean up your space every now and then. You just might save a mouse from obesity.
1. Scutti, Susan. “Could Deleting A Fat Gene Help People Lose Weight?” Medical Daily. N.p., 24 Mar. 2014. Web. http://www.medicaldaily.com/fat10-gene-linked-fat-and-aging-mice-could-deleting-fat-gene-promote-weight-loss-272262
2. University of Colorado Denver. “Gene identified that causes obesity in mice: Deleting gene eliminates obesity, could work for humans.” ScienceDaily. ScienceDaily, 5 March 2013. www.sciencedaily.com/releases/2013/03/130305131304.htm