Researchers discover cellular mechanism that may increase obesity and type 2 diabetes risk
A team of researchers has discovered a signaling pathway in the brain that may play an important role in telling the body that the stomach is full and that it is time to stop eating. The findings could have major implications for the prevention of obesity and type 2 diabetes.
Researchers from the University Texas were looking for possible causes of leptin resistance. This is a hormone that is released in the body after eating and is intended to signal satiety in the brain. However, over time, some people become resistant to the hormone and consequently never receive appropriate signals that indicate they should feel full. This commonly leads to overeating, obesity and diabetes.
However, the team reported in the journal Cell Metabolism
that they may have discovered a cellular pathway that mediates this process. They found that the activation of a certain network of brain cells known as the cAMP-EPAC pathway can induce leptin resistance in the hypothalamus, an area of the brain that is important for feelings of satiety.
Furthermore, when this cellular pathway was blocked from activating, the cells of the hypothalamus remained responsive to the effects of leptin. The researchers said that this is the first time the cAMP-EPAC pathway was associated with this type of metabolic function. Given the preliminary nature of the findings, they said that more research would be needed to confirm their findings.
"These results are potentially interesting and provocative, but the physiological importance remains to be seen," said Joel Elmquist, who led the study. "If, however, this pathway is indeed important, it will offer new insights into the mechanisms that high levels of leptin cause in leptin resistance."
Identifying the biological mechanisms that underlie obesity may be a major step forward in preventing the development of type 2 diabetes, which is increasingly becoming a burden on society.