New research offers potential insight into the connection between cancer, obesity and longevity in humans by showing that genetically modified mice live longer, skinnier and almost cancer-free lives.

There are quite a few differences between mice and humans, especially in regard to the type of fat that’s apparently affected by the genetic tweak, so there’s no way to know if the research could lead to benefits in humans. Even if medications based on the research are developed, no one knows what the side effects in people might be or their eventual cost.

Still, a potential drug “could have two benefits: adding some extra protection against cancer and protecting us from overeating,” said Manuel Serrano, senior group leader at the Spanish National Cancer Research Center in Madrid and co-author of a study appearing in the March issue of Cell Metabolism.

At issue is a gene called Pten that boosts the body’s cancer-fighting powers. Mutations in the gene can contribute to the development of cancer.

The researchers genetically engineered mice to have extra copies of the gene. The mice didn’t suffer from side effects, Serrano said, and they managed to live 15 percent longer than other mice and suffer from less cancer.

He acknowledged, however, that figuring out a mouse’s cause of death can be a challenge.

Mice that ate a high-fat diet also managed to be leaner, suggesting that the genetic tweak affected their ability to gain weight even when they would normally be packing on the extra ounces.

Serrano said the key seems to be the tweak’s effect on something known as brown fat.

Both mice and humans have brown fat, but it’s better understood in mice, he noted. In mice, it appears to burn regular “white fat” and be activated when it’s cold or when the mice eat too much, Serrano said.

“Brown fat is very abundant and active in mice, but in humans it is scarce,” Serrano explained. “At present, it is not known whether pushing the brown fat in humans will have a significant effect in fat burning.”

Serrano said drugs are now in development that tinker with the gene in an effort to fight cancer.

Dr. Aaron Cypess, an assistant professor at Harvard Medical School who studies obesity, said the research appears to be valid and useful.

“There’s a connection being made between tumor-suppressing genes, which prevent cancers from growing, and energy expenditure — consuming calories,” he said. “We know that obesity can lead to cancer in humans. This makes the arrow go the other direction. What it’s saying is that no cancer leads to no obesity.”

There’s a big caveat, however. “While the mouse is a very useful model to understand humans, there are a lot of differences between mice and men,” Cypess said. “Practically speaking, just because something happens in a mouse model doesn’t mean it’s going to happen in a human. We are very different.”

In a related study in the journal, researchers at the University of California, Irvine, found that blocking production of a marijuana-like compound in the brain boosted mice’s metabolism of brown fat. These mice were able to eat more and move less than typical mice, without gaining weight or developing symptoms that can raise the risk of diabetes and heart disease.

More information

For more about obesity, visit the U.S. National Library of Medicine.

SOURCES: Manuel Serrano, Ph.D., senior group leader, Spanish National Cancer Research Center, Madrid, Spain; Aaron M. Cypess, M.D., Ph.D., assistant professor, Harvard Medical School, Boston; March 2012, Cell Metabolism

Last Updated: March 06, 2012