Sunday, June 28, 2009
News, Health + Fitness

Fat hormone could fight breast cancer

Emory researcher says adiponectin may stop spread of cancerous cells

By Diane Loupe

Being fat isn’t healthy, doctors warn us.
 
But a hormone produced by fat cells may help fight breast cancer, according to new research by Emory University researchers. 
 
In research published this month in the scientific journal Oncogene, Emory researcher Dipali Sharma, Ph.D., and her colleagues reported on the remarkable properties of a “guardian angel” hormone called adiponectin. They found this hormone can reduce breast cancer cells’ ability to migrate and invade other tissues.
 
Researchers are eagerly studying adiponectin because it seems to have an effect on a lot of things the body does, including controlling sensitivity to insulin and tumor growth.
 
The hormone appears to protect against the effects of obesity on metabolism, the heart and blood vessels, wrote Sharma, an assistant professor of hematology and medical oncology at the Emory Winship Cancer Institute. Adiponectin is secreted by fat tissue. Sharma believes it could “inhibit the metastatic potential of breast cancer cells.”

In previous studies, researchers have found a link between low levels of adiponectin and an increased risk of breast cancer and more aggressive breast tumors.
 
Sharma’s lab has been studying the molecular links between obesity and carcinogenesis for years. After finding ways that some proteins similar to adiponectin fuel cancer growth, they decided to try to find out how to stop them.

Emory researchers are studying the effects of the “guardian angel” hormone using genetically manipulated mice and human breast tumor samples. “These studies will provide much-needed information for the development of therapeutic strategies,” Sharma says.
 
Sharma and Neeraj Saxena, an  assistant professor of medicine at Emory, along with postdoctoral fellow LaTonia Taliaferro-Smith, discovered that adiponectin boosts the production of the gene LKB1, which suppresses the growth of tumors.
 
The researchers speculate future cancer treatments may make use of substances that can duplicate adiponectin’s effects or maximize the effects of what the body already produces, says Sharma.
 
Although fat cells produce adiponectin, that doesn’t mean gaining more fat produces more of them.  As a person becomes fatter, their adiponectin levels decline, making the levels a good predictor of future risk of developing diabetes, heart disease and cancer, says Philipp Scherer, a professor of internal medicine at University of Texas Southwestern at Dallas. Scherer discovered the hormone in 1994.
 
But what if adiponectin levels did increase when you got fatter?

To find out, Scherer and other researchers genetically engineered mice to produce an overabundance of adiponectin while lacking leptin, a hormone that signals the body to stop eating or to burn energy. The mice gorged themselves and they got fatter, but their bodies behaved as though they were skinny—because they had artificially high levels of the hormone. They just used their fat more healthily. Conversely, Scherer thinks that in people who have low levels of adiponectin, fat is stored in dangerous places such as the liver, heart and muscle tissues, where it can pave the way for disease.

“The message isn’t that it’s good to be obese, but that expanded fat mass, when stored in the right places, can help prevent diabetes and reduce the risk of heart disease,” Scherer stated in a news release after his research was published in 2007 in the Journal of Clinical Investigation.

“More than 66 percent of American adults are overweight or obese, so most people have excess caloric intake. We need to find ways to deposit these calories in the least harmful places, because the fat has to go somewhere,” Scherer says. “For instance, people with excess weight around their abdomen run a higher risk of heart disease and diabetes than those who have excess weight in the thighs.”
 
Today, Sharma’s lab is studying how adiponectin works in both normal and obese conditions. She believes her research findings will help provide more treatment options for cancer patients. “We will able to use this information to develop therapeutic strategies” to fight the spread of cancer cells, she says.
 
The class of anti-diabetic drugs known as thiazolidinediones has been shown to activate adiponectin, so they represent one possible option for breast cancer treatment, Sharma says. However, they have a complicated set of side effects on bones, the liver and heart, and can cause fluid retention. Another option may be to administer adiponectin itself, or a related protein known as osmotin.
 
Sharma says human treatments for cancer using adiponectin or its analogues could be available within a decade. SP