Research around how the body's fat levels are regulated and ways in which they might be manipulated has uncovered numerous potential fat switches. The latest is a particular protein that has long been known to regulate protein synthesis and has now been demonstrated to also control fat levels in worms. This has lead researchers at the University of Southern California (USC) to believe that the version found in the human body could provide a new target for fat-fighting pharmaceuticals.
Scientists have studied the MAF1 protein for some time, but this has largely been limited to its ability to control the production of other proteins. In a study conducted at the USC Davis School of Gerontology, scientists found that the protein is actually capable of much more.
“We’ve known about MAF1 for over a decade, but so far people have only studied it in single cells, where it is known to regulate protein synthesis,” says Sean Curran, assistant professor at USC Davis and on of the study's co-authors. “No one really looked at its effect on the whole organism before.”
Curran and his team modified the MAF1 levels in transparent worms known as C. elegans and found that adding a single copy of the gene expressing MAF1 lowered stored lipids by 34 percent. Conversely, lowering MAF1 levels saw lipids boosted by 94 percent.
The fact that the version of MAF1 in humans has the same protein-producing properties leads the researchers to suspect that it, too, could control the storage of fat cells. If this proves correct, the protein could offer a target for a new breed of pharmaceutical treatments for obesity and weight-related health problems. One other notable finding was that the MAF1 protein can also impact on lipid metabolism in cancer cells, suggesting that it could be used in suppressing cancer cells.
Curran's team next plans to test the fat-fighting ability of MAF1 in mice. If successful, they hope to eventually investigate its potential in humans.
The research findings were published in the journal Cell Reports.
Want a cleaner, faster loading and ad free reading experience?
Try New Atlas Plus. Learn more