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Sydney: a set of brain cells found by the Garvan Institute for Medical Research increases appetite when there is a persistent surplus of energy in the body, as excess fat storage in obesity.
The results of the study have been published in the journal Cell metabolism. The researchers observed that not only did these cells create the Appetite Stimulating Chemical NPYbut they also made the brain more sensitive to the molecule, increasing appetite even more.
“These cells trigger changes in the brain that make it more sensitive even to low levels of NPY when there is excess energy in the body in the form of excess fat – stimulate the appetite during obesity”, explains the professor Herbert Herzoglead author of the study and visiting researcher at Garvan.
“Our study addresses a long-standing question about how appetite is controlled in obesity and has the potential to take therapy development in a new direction.”
Obesity is a major public health problem and a disease that affects more than one in 10 adults and increases the risk of developing other chronic diseases, such as diabetes or heart disease. While many factors can influence the development of obesity – excessive accumulation of fatty tissue in the body – dietary habits and levels of physical activity are key factors.
“Our brain has complex mechanisms that sense the amount of energy stored in our body and adjust our appetite accordingly. One way to do this is by using the molecule NPY, which the brain naturally produces in response to stress, such as hunger, to stimulate eating,” Professor Herzog said.
“When the energy we consume is less than the energy we expend, our brain produces higher levels of NPY. When our energy intake exceeds our expenditure, NPY levels drop and we feel less hungry. “There is a prolonged energy surplus, such as excess body fat in obesity, NPY continues to stimulate appetite even at low levels. We wanted to understand why.”
In mouse models of obesity, the researchers studied brain cells called neurons that produced NPY and found that 15% of them were different – they did not shut down NPY production during obesity.
“We found that under conditions of obesity, appetite was primarily driven by NPY produced by this subset of neurons. These cells not only produced NPY, but also sensitized other parts of the brain to produce additional receptors or ‘docking stations’ for the molecule – stimulate the appetite even further,” Prof. Herzog explains.
“What we discovered is a vicious cycle that disrupts the body’s ability to balance its energy intake with energy storage and enhances the development of obesity.”
“Our brain is wired to resist energy deficiencies or weight loss because it sees this as a threat to our survival and triggers mechanisms that increase our appetite so that we seek out food. As we have now discovered , this happens even when we have excess energy stored in the body,” Professor Herzog explained.
The researchers say their discovery opens up the possibility of blocking additional, more sensitized NPY receptors as a novel approach to developing anti-obesity drugs.
“Our discovery helps us better understand the brain mechanisms that interfere with balanced energy metabolism and how they can be targeted to improve health,” Professor Herzog said.
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