Geschatte leestijd: 2 minutenHunger Cells Influencing Appetite? Researchers Identify New Brain Cells
“Hunger Cells”
Researchers from Rockefeller University have identified two populations of brain cells that play a significant role in appetite regulation [1]. These two types of cells are located in a part of the brainstem called the nucleus raphe dorsalis. This is a new clue that hunger and appetite are complex biological behaviors influenced at multiple sites in the brain. Understanding the various factors that determine appetite could translate into better methods to combat obesity at the neural level.
Previous research from Rockefeller in 1994 introduced the world to the ‘hunger hormone’ leptin. Leptin works by suppressing hunger through neurons in the hypothalamus. Administering leptin to people with a rare leptin deficiency has resulted in significant weight loss. However, in many overweight individuals, it has yielded little results. Leptin resistance is often associated with obesity. The researchers at Rockefeller believe that with their new insights, it may be possible to bypass this leptin resistance by modifying the activity of certain neurons.
Using a self-developed imaging technique, the researchers examined the brainstem in mice. They found that it became active when the mice became hungry. When they then observed mice that had eaten to satiety, they saw a different pattern of activity. This is a clear indication that the neurons in this region play a role in appetite.
They then used genetic analysis of the activated cells to see which of the different types of neurons were involved in this process. They found that neurons activated in hungry mice released glutamate, while in satiated mice, neurons activated released GABA. Both are neurotransmitters, signaling molecules that nerve cells use to communicate. This could mean that they simply ‘go along for the ride’ of the appetite process or form an important chain in it. The researchers suspect the latter.
Hunger Cells Influencing Appetite
They then took it a step further. They used two established methods to activate specific neurons: chemically and optically. With this, they activated the ‘satiety neurons’ that release glutamate in overweight mice. This suppressed appetite and caused them to lose weight. This also provided evidence that these neurons form an important chain in the appetite process.
Activating the neurons that release GABA had the opposite effect, increasing the amount of food the mice ate. Activating these ‘hunger neurons’ also caused the ‘satiety neurons’ to be deactivated.
Finally, they also looked at what happened when they deactivated the ‘hunger neurons’. They found that prolonged deactivation of these neurons led to significant weight loss in overweight mice.
More hope for the future!
Reference
- Alexander R. Nectow, Marc Schneeberger, Hongxing Zhang, Bianca C. Field, Nicolas Renier, Estefania Azevedo, Bindiben Patel, Yupu Liang, Siddhartha Mitra, Marc Tessier-Lavigne, Ming-Hu Han, Jeffrey M. Friedman. Identification of a Brainstem Circuit Controlling Feeding. Cell, 2017; 170 (3): 429 DOI: 10.1016/j.cell.2017.06.045
