Washington: Scientists for the first time have managed to transform static white fat into brown fat that burns off more energy. They say that it can be a breakthrough which may lead to better treatments for people suffering from obesity.

Researchers at the Johns Hopkins University School of Medicine found that knocking down the expression of an appetite-stimulating protein not only helps cut calorie intake and weight but also it turns white fat into brown one.

“If we could get the human body to turn ‘bad fat’ into ‘good fat’ that burns calories instead of storing them, we could add a serious new tool to tackle the obesity epidemic in the United States," said study author Sheng Bi, an associate professor at the Johns Hopkins University School of Medicine.

According to scientists, the body produces two fats oradipose tissue. The white one, called the storehouse for the extra calories we eat, ends up being stored in the body, while the brown fat which generates body heat in animals or newborns is considered as good fat.

For the study, published in the journal Cell Metabolism, Bi and his team wanted to see whether suppressing neuropeptide Y (NPY), the appetite-stimulating protein, in the dorsomedial hypothalamus of the brain would decrease body fat in rats.

Located just above the brain stem, the hypothalamus helps standardise thirst, hunger, body temperature, water balance and blood pressure.

For five weeks, the two groups of rats were fed a regular diet, with one group also treated with a virus to inhibit NPY expression and the other left as a control group.
   
It was found that the treated group weighed less than the control group, showing that suppression of NPY reduced eating.

Then, researchers split the groups into two, creating four sets of rats. One of the treated groups of rats and one of the control groups were fed a regular diet while the other treated and control groups got a high-fat diet.

Of the rats on the regular diet, the control group weighed more at the end of 11 weeks than those rats in which hypothalamic NPY expression was knocked down.

In the high-fat group, the control group rats became obese, while those rats in which NPY expression was silenced gained less weight.

The results made sense, given that NPY has been shown to stimulate eating, said Bi. The less NPY, the less the rats would eat, his team hypothesised. But, the team was surprised when they checked the fat content of rats after death.

In the groin area of the NPY rats, they found not the expected white fat, but the telltale signs of brown fat in its place.
They confirmed this change by looking at levels of mitochondrial uncoupling protein-1, or UCP-1, through which brown fat burns to produce heat.

They used this protein as a marker to decide that the fat that should have been white was instead brown.
Bi said the transformation from white to brown resulting from NPY suppression may be due to activation of brown fat stem cells contained in white fat tissue.

While brown fat seems to vanish in humans as they emerge from infancy, the brown fat stem cells may never vanish and may just become inactive as people age.

(Agencies)