Scientists studying obesity in mice have discovered a new type of brain cell that increases appetite, even after long periods of satiety.
Neuropeptide Y neurons are the focus of many studies of metabolic syndromes. They are most abundant in the hypothalamus region of the brain called the arcuate nucleus, producing powerful neurotransmitters that stimulate appetite and delay satiety.
For many years, only one type of neuron was thought to express neuropeptide Y (NPY), the molecule that gives NPY neurons their name, in this part of the brain.
But as it turns out, another group of neurons hidden in the hypothalamus also produces motivation – not always when it’s beneficial.
Under fluorescent microscopy, a team of international scientists claims to have found “a large number of NPY-positive neurons”, which have not yet been counted.
Unlike other neurons that produce NPY, this new group does not express the neurotransmitter AgRP, which is why the newly described neurons are described as ‘AgRP-negative’.
In mouse models, these neurons respond quickly and strongly to fasting, expressing neuropeptide Y and promoting food intake.
On the flip side, when more energy is stored in the mouse’s body for a longer period of time, these same neuropeptides continue to express the neuropeptides that increase attention.
“We found that under obesity, appetite is strongly regulated by NPY produced by a subset of neurons,” said Herbert Herzog, who studies the neurobiology of eating disorders at the Garvan Institute of Medical Research in Australia.
“These cells not only secrete NPY but also stimulate other parts of the brain to create more receptors or ‘repositories’ of the molecule – a greater appetite.”
It’s a challenge, and it’s one that Herzog and his colleagues want to learn more about.
There is no guarantee that the specific processes of energy consumption and energy consumption will be adapted to humans – there may be other appetite-stimulating neurons that can be found – but animal models are a useful way to increase psychological research.
Previous research in mice has shown that when AgRP-positive NPY neurons are blocked in the brain, there is a severe decrease in food intake, sometimes leading to starvation.
But Herzog and colleagues say these earlier experiments “missed or ignored the contribution” of other NPY-producing neurons they had just discovered.
In the experiment, AgRP-negative neurons were more sensitive to a drop in energy than AgRP-positive neurons, and they responded more strongly to stimuli that stimulated appetite.
When scientists suppressed AgRP-negative NPY neurons in the brains of mice, eating and postprandial weight gain were significantly reduced.
“Our discovery helps us better understand the brain’s mechanisms that affect energy metabolism and how they can be used to improve health,” said Herzog.
This study was published in Cell Metabolism.
