By Simply Deleting A Gene, Researchers Eliminate Obesity In Mice
April Flowers for redOrbit.com – Your Universe Online
A research team from the University of Colorado School of Medicine and The Obesity and Metabolism Laboratory at Tufts University has discovered that deleting a specific gene in mice prevents them from becoming obese, even if they are fed a high fat diet. The team believes this finding has the potential to be replicated in humans.
“When fed a diet that induces obesity these mice don’t get fat,” said James McManaman, Ph.D., vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine. “It may be possible to duplicate this in humans using existing technology that targets this specific gene.”
The National Institutes of Health (NIH) and the US Department of Agriculture funded the study, which lasted two years. The findings were published in a recent issue of the Journal of Lipid Research.
The researchers created a strain of mice missing the Plin2 gene. Plin2 produces a protein that regulates fat storage and metabolism. It was immediately apparent that the mice were resistant to obesity.
Normal mice that are fed a high fat diet will usually eat voraciously, taking in as many calories as they can. The mice that were missing the Plin2 gene, however, showed an unusual restraint and ate considerably less. The researchers found that they were also more physically active.
The researchers found that the fat cells in these mice were 20 percent smaller than the average mouse as well. The cells also did not show the kind of inflammation of tissue typically associated with obesity. The mice missing the Plin2 gene also displayed a lack of obesity-associated fatty liver disease, common in obese humans and rodents.
“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 also suggested that the absence of the gene may cause fat to be metabolized faster.
“Now we want to know why this works physiologically,” McManaman said. “We want to better understand how this affects food consumption.”
The researchers believe that understanding Plin2′s involvement in the control of energy balance will provide new insights into “the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges.”
Humans also have the Plin2 gene, making these findings potentially significant for us as well.
“It could mean that we have finally discovered a way to disrupt obesity in humans,” he said. “That would be a major breakthrough.”