Recent research has shown that a signaling pathway in fat cells turning white fat to brown fat may be the key for more promising treatments for obesity. These findings were revealed by researchers from the Perelman School of Medicine at the University of Pennsylvania. Their findings were reported in the online issue of Genes & Development.
White fat cells are ordinary fat cells that store energy yet when in excess they lead to obesity and other medical conditions such as diabetes and heart disease. Brown fat which is also termed as baby fat do the opposite of what white fat cells dothey burn energy so that they can generate heat to protect the body from cold while also preventing obesity and diabetes. Brown fat is abundant in babies while white fat is common in adults. The recently discovered signaling pathway was able to activate a browning program that can transform white fat cells into brown fat cells, making them energy burners.
The study's senior author, Zoltan P. Arany, MD, PhD, an associate professor of Cardiovascular Medicine commented that it is possible that this signaling pathway can be targeted later on by a drug to convert white fat to brown fat and therefore treat obesity.
It is a known fact that around 36 percent of adult Americans are obese and around 10% of them have diabetes.
Brown fat and browning program
In this study, the researchers found out that this browning program, white fat cells were suppressed by a protein known as FLCN. This protein performs its functions with the help of a major cellular signaling hub composed of a protein complex known as mTOR. When FLCN interacts with mTOR, the browning program is switched off by the prevention of a protein called TFE3 from entering the cell's nucleus.
The researchers were able to show that by deleting the FLCN gene in the white fat cells of mice, TFE3 will migrate into the cell nucleus and bind with DNA to activate a key regulator of cell metabolism known as PGC-1 beta. This process then turns on the set of genes that trigger the browning program.
Mice which had the FLCN deleted had their white fat cells become visibly browner and these fat cells began to develop more mitochondria which are tiny oxygen organelles that supply chemical energy to cells and convert energy to heat in brown fat cells. These mitochondria also have altered cellular structures that increase their capacity for consuming oxygen. They also developed a distinct pattern of gene expression that made the fat cells more like brown fat cells.
The researchers claimed that they were able to reproduce this browning effect by forcing the over expression of PGC-1 beta in white fat cells of mice. A drug that boosts the function of PGC-1 beta or its target genes may serve as a treatment that could activate the browning program to treat obesity, diabetes and other related diseases.