There are two types of fat cells in our fat tissue: brown fat and white fat cells. When brown fat cells are stimulated, they can release the energy in the cells through heat. Certain conditions can stimulate brown fat into its exothermic capacity, such as being exposed to cold temperatures. Other substances are being investigated for their abilities to stimulate brown fat into burning mode.
Recent research into brown fat has found a pathway that can enhance their exothermic properties without causing the cells to hold onto more fat. Unfortunately, many of the known methods which stimulate the energy-burning of brown fat into heat causes more white fat cells to accumulate. This pathway, discovered in mice, offers an alternative that unleashes the energy potential of brown fat without simultaneously increasing harmful stores of white fat cells.
The key to this pathway is in precursor proteins. The scientists at the Joslin Diabetes Center found two proteins which belong to a family of proteins called fibroblast growth factors. Fibroblast growth factors which are involved in cell development and growth. Two specific fibroblast growth factors are involved in enhancing the brown fat cells.
The researchers found that two of the fibroblast growth factors enhanced brown fat in different ways; one stimulated brown fat through cold temperatures and the other through exercise. They were able to confirm that the same pathway is present in human fat tissue and also made some interesting connections.
One of the receptor proteins that is activated by the fibroblast growth factors are found in higher levels in human fat tissue (both brown and white), and one particular expression of the fibroblast growth factor is correlated to reduced BMI (body mass index) and insulin resistance. The team hopes that if they can find was to activate this particular pathway in humans, they will be able to find some solutions to metabolic and insulin-related conditions.
Farnaz Shamsi, Ruidan Xue, Tian Lian Huang, et al. FGF6 and FGF9 regulate UCP1 expression independent of brown adipogenesis. Nature Communications, 2020; 11 (1) DOI: 10.1038/s41467-020-15055-9