Skinny mice. That’s what OMRF scientist Lorin Olson, Ph.D., created when he added a particular gene to the animals.
It was not the outcome the researcher expected. But it could hold the key to understanding how humans create fat—and whether a drug might one day stop this process.
Olson, a developmental biologist who studies organ growth and regeneration, added the gene called PDGFRbeta to laboratory mice with the expectation that this would cause them to develop cancer. They didn’t. Yet that was not the most unexpected outcome of the research.
Instead of developing cancer, Olson found that the cells responsible for making connective tissue—including tendons, cartilage and fat—did not become fat cells. The new research appears in the scientific journal Developmental Cell.
“The juvenile mice still had brown fat, which is used to burn energy, but they didn’t have any of the white, ‘jiggly’ fat that usually begins to appear right after birth,” said Olson, an assistant member of OMRF’s Immunobiology and Cancer Research Program. It wasn’t immediately apparent why the young mice weren’t making white fat, he said.
“It’s always exciting when you find something unexpected like this,” he said. “But this result doesn’t give us a definitive answer—it poses a lot of new questions.”
Olson said the next phase of his research is finding out what the cells that wouldn’t become fat would turn into instead. It is possible that the same added gene in adult mice would cause cancer cells, as they had originally hypothesized.
As for the potential for a weight-loss therapeutic, the key will be in understanding how the added gene affects other genes that are important for fat formation, he said.
“If we can map the process that eventually ends in fat growth, we might be able to come up with a way to safely disrupt that chain of events,” he said. “This finding is a good start on unlocking those secrets.”
The research was initiated by Olson when he was a postdoctoral fellow with Philippe Soriano, Ph.D., of the Mount Sinai Medical Center in New York and was completed at the Oklahoma Medical Research Foundation. Olson and Soriano are the co-authors of the study.
The research was funded by grants from the National Institute of Child Health and Human Development and the American Cancer Society.