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FAT10 Gene tied to Body fat and Aging in Mice, Study Reports

Update Date: Mar 24, 2014 03:01 PM EDT

One particular gene could be linked to the body's immune system and metabolism. In a new study, researchers examined the effects of removing this particular gene, known as the FAT10 gene. They found that in mice models, the deletion of the gene leads to slower aging and less body fat.

The research team headed by scientists from the Jean Mayer United States Department of Agriculture Human Nutrition Research Center (USDA HNRCA) on Aging at Tufts University and Yale University School of Medicine examined previous studies conducted on the relationship between gene expression and fat tissue.

"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," said co-author Martin S. Obin, Ph.D., an adjunct scientist in the Functional Genomics Core Unit at the USDA HNRCA at Tufts University. "Turning off the FAT10 gene produces a variety of beneficial effects in the mice, including reduced body fat, which slows down aging and extends lifespan by 20 percent."

The researchers had observed two sets of mice. In the first group of mice, the FAT10 gene was activated. These mice aged normally and had increased fat. In the other group of mice, the FAT10 gene was deleted. These mice ended up eating more food and burned more fat tissue at a faster pace. The mice without the gene also responded better to insulin, which reduced circulating insulin levels, lowered the risk of type 2 diabetes and extended lifespan. Despite this finding, the researchers stated that deleting the FAT10 gene might not be beneficial in the real world.

"Laboratory mice live in a lab under ideal, germ-free conditions," said Obin, who is also an associate professor at the Friedman School of Nutrition Science and Policy at Tufts University. "Fighting infection requires energy, which can be provided by stored fat. Mice without the FAT10 gene might be too lean to fight infection effectively outside of the laboratory setting. More research is needed to know how to achieve that balance in mice and then hopefully, at some point, people."

The findings were published in the Proceedings of the National Academy of Sciences (PNAS).

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