Glutton's Dream Come True? Scientists Discover Deleting "Fat Gene" Makes Mice Immune to Obesity
Imagine eating all the ice cream, burgers and pizza to your heart's content and not gaining a pound. Scientists claim they have found a way to turn this glutton's fantasy into reality in mice.
A new two-year study found that deleting a gene in mice made them resistant to obesity, even when placed on a high fat diet. Researchers believe that the latest findings, published in the Journal of Lipid Research, could also apply to humans.
Researchers from the University of Colorado School of Medicine said that mice fed a high calorie diet will usually eat "voraciously," but mice with the disabled "fat" gene exhibited "unusual restraint" to high fat foods and were also more active.
"When fed a diet that induces obesity these mice don't get fat," lead author Professor James McManaman of the University of Colorado School of Medicine said in a news release.
"It may be possible to duplicate this in humans using existing technology that targets this specific gene," he added.
McManaman and his team created a strain of mice without the Plin2 gene. Researchers say that the Plin2 gene, which is also in humans, produces a protein that regulates fat storage and metabolism.
Surprisingly, researchers immediately found that mice without the Plin2 gene appeared to be resistant to obesity.
They found that not only did the mice with the deleted Plin2 gene show "unusual restraint" to high calorie food and were more active, their fat cells were also 20 percent smaller than normal nice and did not show the kind of inflammation usually associated with obesity.
Furthermore, researchers found that obesity-associated fatty liver disease, which is common in obese humans and rodents, was absent in mice without the Plin2 gene.
"The mice were healthier," McManaman said.
"They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells," he explained.
Researchers believe that the removal of the Plin2 gene caused fat to be metabolized faster. McManaman and his team believe that deleting the gene in people could lower the risk of heart disease and diabetes.
"It could mean that we have finally discovered a way to disrupt obesity in humans," he said. "That would be a major breakthrough."
Researchers wrote in the study that understanding how the Plin2 gene is involved in the control of energy balance will provide new insights into the "the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges".
McManaman said the next step for him and his team is to better understand how the gene alteration works physiologically and how it affects food consumption.
The study was sponsored by the National Institutes of Health and the U.S. Department of Agriculture.