You always have room for a sugary treat
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Even after eating a large meal, most people can still find room for sweets. Now, research in mice shows that the neurons responsible for feelings of fullness are also those that trigger sugar cravings. In other words, there seems to be a neurological basis for our love of dessert.
Previous studies have shown that naturally occurring opioids in the brain play a crucial role in sugar cravings. The main producers of these opioids are neurons located in a brain region that regulates appetite, metabolism and hormones, called the arcuate nucleus of the hypothalamus. These cells, known as pro-opiomelanocortin (POMC) neurons, also control feelings of satiety after eating.
To understand whether the cells have a role in sugar cravings, Henning Fenselau at the Max Planck Institute for Metabolism Research in Germany and his colleagues traced the opioid signals the POMC cells send in the brain. They did so by bathing brain slices from three mice in a fluorescent solution that binds to receptors of these opioids.
The brain region with the highest density of these receptors was the paraventricular nucleus of the thalamus (PVT), known to regulate feeding and other behaviours. That suggested that sugar cravings were related to communication between these two brain regions – the arcuate nucleus of the hypothalamus and the PVT.
So, the researchers monitored the activity of neurons in these regions as mice ate their usual food. After 90 minutes, the animals seemed to be full – they only nibbled at additional food. At that point, the team gave them a dessert of sugary chow.
On average, neuronal activity between the brain regions roughly quadrupled while mice ate their dessert compared with when they ate their regular meal. The spike began before they even started eating the sweets, suggesting this brain pathway dictates sugar cravings.
The researchers confirmed this using a technique to switch cells on and off with light, called optogenetics. When they inhibited signals from POMC neurons to the PVT, the mice consumed 40 per cent less dessert.
“The cell types, which are extremely well known for driving satiety, also release signals that cause the appetite for sugar, and they do so particularly in the state of satiety,” says Fenselau. “This would explain why animals – humans – over-consume sugar when they’re actually full.”
We don’t know why this pathway evolved in animals. It may be because sugar is more easily converted into energy than other sources like fats or proteins, says Fenselau. Eating dessert could thus be almost like topping up your gas tank.
He hopes this research could lead to new treatments for obesity, though he acknowledges that hunger and cravings are complicated in day-to-day life. “There are so many other pathways in the brain that, of course, could override this. We have found this pathway, but how it plays together with many others is something we don’t know at the moment.”
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