(Defeat Diabetes® News) -- Obesity is an incredibly serious global problem, being linked to numerous deadly diseases, including diabetes. Awareness campaigns, novel treatments, fad and medically accepted diets, and more, have all tried to curtail the obesity epidemic. According to McGill researchers, however, the key to fighting obesity might be inside of some special worms. 

 

Hibernation is possible due to the ability to store energy and slow metabolism. A certain type of roundworm, known as Caenorhabditis elegans, goes through the common hibernation process, sometimes for upwards of six months, but some die after only a few days of hibernation. It's been found by researchers that this strange occurrence is due to a mutation that disallows the slowing of the metabolism, which burns up all the extra energy stored as fat. It's speculated, however, that this unwanted fat-burning mechanism in C. elegans, may have an extension to humans as a treatment for obesity.

 

C. elegans hibernation process is called "dauer," which is when they "shut down everything energy-consuming, which includes foraging, cell division and reproduction." What makes their process unique though is the large amount of energy reserves they accumulate before dauer, which allow normal C. elegans to live many month in dauer. The "mutant" worms die within a few days though. Dr. Richard Roy explains why: "They cannot adjust their metabolism correctly. They store up their six-month lipid reserves, but as soon as they shift into dauer they use them up within a few days. This is because they lack an enzyme that blocks the activity of a very important triglyceride lipase. Without this regulation the lipase burns up all the fat it encounters and destroys the worm's energy reserves."

 

While worms in themselves might be fun to research for scientists, it's the potential human application that might make this discovery worthwhile. Dr. Roy explains that, based on his discovery, "I think we should start looking at the enzymes involved in this cascade, particularly in obese individuals. They are likewise accumulating lipids, but in a reverse situation to C. elegans, this enzyme isn't recognizing it, or something is blocking its function. We're making the case that we can uncouple this enzyme from its normal regulation. If we could develop drugs to do that selectively in fatty tissue, we'd be able to chew up all the fat." Simply put, separating this enzyme that stores excess energy in humans, may allow excess fat to be quickly eliminated. Dr. Roy's colleague at McGill, Dr. Robert Sladek expresses interest and optimism, saying, "tt will be exciting to see whether this pathway that controls energy storage and lifespan in worms plays a similar role in humans. The implications for patients with obesity and diabetes might be quite far-reaching."