Scientists have discovered a new type of brain cell that increases appetite in mice even when their bodies are satiated, according to a recent study. The research, conducted by an international team of scientists, found an abundance of neuropeptide Y neurons in a part of the brain’s hypothalamus called the arcuate nucleus. These neurons produce powerful neurotransmitters that stimulate appetite and delay the feeling of fullness, making them a focus for research into metabolic syndromes.

Newly Discovered Neurons

Until recently, it was thought that only one type of neuron produced neuropeptide Y (NPY) in the arcuate nucleus. However, using fluorescent microscopy, the scientists discovered another group of neurons that also produced appetite-boosting molecules, even when it was not beneficial to do so. They found that these NPY-positive neurons responded to fasting conditions, promoting food intake by expressing neuropeptide Y. Conversely, when excess energy was stored in the mouse body for extended periods, these same neurons continued to produce neuropeptides that increased appetite. These newly discovered neurons were described as ‘AgRP-negative’ because they did not co-express the neurotransmitter AgRP, which is found in other NPY-producing neurons.

Obesity and Appetite

The researchers found that these AgRP-negative neurons played a significant role in driving appetite under obese conditions. Not only did they produce neuropeptide Y, but they also sensitized other parts of the brain to produce additional receptors or ‘docking stations’ for the molecule, resulting in even stronger appetite-boosting effects. This created a vicious cycle that the researchers are keen to study further. Although these mechanisms have only been observed in mice, they may provide useful insights into the neurological factors that contribute to appetite and obesity in humans.

Implications for Research

Previous studies on mice have shown that restricting AgRP-positive NPY neurons in the brain can significantly reduce food intake, sometimes to the point of starvation. However, Herzog and his colleagues argue that these studies overlooked the contribution of the newly discovered NPY-producing neurons. Experiments showed that AgRP-negative neurons were more sensitive to drops in energy than AgRP-positive neurons and responded more strongly with appetite-boosting measures. When scientists suppressed these neurons in mouse brains, food intake and post-meal weight gain were significantly reduced. The researchers believe that their discovery could help improve our understanding of the mechanisms in the brain that interfere with a balanced energy metabolism, leading to obesity and other eating disorders.


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