Finding a way to eat delicious foods (such as burgers and pizza) and stay thin, would be a dream come true for many Americans, particularly for seniors. As we age, our metabolism continues to slow down, making it easier and easier to gain weight. It may seem that eating the foods we enjoy, becomes more of a distant memory as time goes on. But, medical science may have found a way to defy biology, according to a new study conducted by The Faculty of Health and Medical Sciences at the University of Copenhagen.
Lipid (Fat) Storage
The human body has an ingenious system of storing fat (as many people over 55 know full well). Adipose (fat) tissue can expand and contract, in response to fluctuations in the availability of calories. This mechanism, called “adipose plasticity” is required for the body’s ability to maintain balance and equilibrium. Adipose plasticity evolved over millions of years in mammals, in response to commonly facing a scarcity of food.
In fact, there are many biological mechanisms that ensure we keep much of the fat in the diet we eat, stored for future use, in case there is no food readily available. It’s part of a very effective survival mechanism in humans, as well as in animals.
Given the caloric excess in the Western diet today, this highly efficient fat storage mechanism may now present more of a metabolic liability, than a survival asset. But, a recent study, performed on mice, may have found a way to completely block the mechanism that causes excess fat storage and results in obesity. The scientists hope the research may eventually result in aiding in the development of an effective new treatment for weight gain and obesity.
In the study, the researchers found a way to delete an enzyme that is needed to store fat in mice. The enzyme is called “NAMPT,” and it was found in the fat tissue of mice. Genetically deleting the enzyme, rendered the mice completely resistant to becoming overweight—even when eating a very high fat diet. The group of mice in the study, lacking NAMPT also had better glucose (blood sugar) control than normal mice, when eating a high fat diet.
“We gave the mice a diet that more or less corresponds to continuously eating burgers and pizza. Still, it was impossible for them to expand their fat tissue. Our ultimate goal is that by understanding these fundamental underpinnings of how we become obese, we can apply our finding to the development of novel treatment strategies for metabolic disease,” says Karen Norgaard Nielsen, Ph.D. student at the Novo Nordisk Foundation Center for Basic Metabolic research and lead study author.
The study findings were reportedly in line with the same results discovered in humans. In fact, other studies found that large amounts of the enzyme NAMPT in the human body, were linked with obesity. However, this study provides the very first conclusive evidence that the enzyme NAMPT is required as part of the process of becoming overweight or obese. Researchers involved in the study have made a bold statement that the lack of NAMPT fully protects against obesity.
Although researchers do not believe that lowering NAMPT in humans is a viable treatment option yet (due to health risk potentials) the study may be the first, of many future discoveries, which paves the way to a safe and effective treatment for obesity and metabolic diseases.
University of Copenhagen