TUESDAY, March 6 (HealthDay News) -- 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
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
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,
"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
"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.
For more about
obesity, visit the U.S. National Library of Medicine.
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