The study showed that adenosine, a metabolite released when the body was under stress or during an inflammatory response, stopped the process of adipogenesis, when adipose (fat) stem cells differentiated into adult fat cells.
The findings indicated that the body's response to stress, potentially stopping the production of fat cell development, might be doing more harm than good under conditions of obesity and/or high levels of circulating blood fat.
The process is halted due to a newly identified signaling from an adenosine receptor, the A2b adenosine receptor (A2bAR) to a stem cell factor, known as KLF4, which regulates stem cell maintenance. When A2bAR is expressed, KLF4 level is augmented, leading to inhibition of differentiation of fat stem cells. The correlation between these two factors leads to an interruption of fat cell development, which could result in issues with fat storage within the cells and it getting into the bloodstream.
Katya Ravid, DSc/PhD, said that it might seem counterintuitive, but the body needs fat tissue in order to function properly, and certain biochemical cellular processes were necessary for this to happen.
He further explained, however, the study indicated that a dysfunction resulting from stress or inflammation could disrupt the process of fat tissue development, which could have a negative impact on processes dependent on proper fat cell homeostasis.