Americans love to eat, and we seem to be drawn to some of the most greasy and unhealthy foods.  As a result we have one of the highest obesity rates in the world.

There are thousands of diet plans on the internet, some of which may work and many that don’t.  There are also medications such as Xenical which are proven to help lose weight.  For extreme cases of obesity, it becomes necessary to have surgery to help shed the pounds.

But what if your body was unable to retain fat in the first place?  Wouldn’t it be nice to be able to eat whatever you want and never gain weight?

The University of Texas Health Science Center at Houston may have done just that.  Recent stem cell research has shown that it is possible to prevent stem cells from producing the belly fat that is plaguing so many Americans.

The Scientists used a groundbreaking new method for targeting fat-generating stem cells.  This method could eventually be used to slow the cells’ ability to store fat.  Small artificial proteins were used in mice to identify the adipose stem cells responsible for fat storage in the body of both mice and humans.

Alexes Daquinag, Ph.D., the study’s first author and postdoctoral fellow at the UTHealth Medical School, said, “In obesity, you have an overgrowth of white adipose tissue. It is made of adipocytes (fat cells) and one way to stop obesity is to target the progenitor cells — adipose stem cells.”

“Helping people lose weight might also reduce their risk of cardiovascular diseases, certain types of cancer, Type 2 diabetes and other obesity-related diseases,” said Kolonin, director of the study at the University of Texas Health Medical School.

Now that the scientists are able to target the source of these fat cells in the body, they will be able to control and eliminate them when they are causing a problem.   The next step will be to develop compounds that will target these specific adipose stem cells.  By getting rid of these cells, they may be able to provide long-term fat loss without a need for dieting or surgery.