Fat or adipose tissue is mainly of two types – white and brown adipose tissue (WAT and BAT), based on their color. WAT stores energy, while BAT generates body heat. BAT is abundant in newborns and hibernating mammals since they generate heat and prevent them from shivering in the cold. In newborn infants, brown fat makes up about 5% of the body mass and is located on the back, along the upper half of the spine and towards the shoulders. It is of great importance since they avoid hypothermia, which is essential in newborn infants.
Recent studies have shown that mice and humans exposed to cold have increased brown fat. However, further studies have to be performed on humans to determine the long term effects of cold exposure and brown fat accumulation. Various studies are also being done on understanding conversion of white to brown fat (‘beige fat’).
UCP-1, PGC1a and PRDM16 have already been shown to be responsible for brown fat conversion as these two genes are highly expressed in brown adipose tissue. The present study identifies the protein responsible for activation of UCP1 as well as PGC1a. The researchers have identified the cold-inducible protein, Zfp516 (zinc finger protein 516) to be responsible to activate UCP1 transcription to promote browning of white fat and development of white fat.
According to their results, Zfp516 can be induced by cold and sympathetic stimulation and directly binds to the proximal region of the UCP1 promoter and interacts with PRDM16 to activate UCP1 transcription. They also showed that over-expression of Zfp516 in adipose tissue can promote browning of WAT even at room temperature (no need for cold induction). This results in increase in body temperature, energy expenditure and also prevents diet-induced obesity.
Zfp516 can promote brown adipogenesis and suppress myogenesis. Overall, their studies suggest that Zfp516 (even at room temperature) can be of therapeutic value to fight obesity.
The original publication can be accessed here.