Why does our desire to keep eating overpower the signal from our brain saying we are full? A new study has shown that the reason for this involves a battle between two neighbouring groups of brain cells, in which the brain’s opioid system also has a role. The study was carried out on mice; however, scientists believe that this will help us to understand similar mechanisms in humans. Professor Huda Akil, a neuroscientist in the Department of Psychiatry at the University of Michigan Molecular and Behavioural Neuroscience Institute in Ann Arbour, explains the study; “Our work shows that the signals of satiety — of having had enough food — are not powerful enough to work against the strong drive to eat, which has strong evolutionary value.”
Throughout the study, Professor Akil and her colleagues focused on two small groups of adjacent nerve cells, or neurons, in the hypothalamus, a small brain region that is involved in several functions, such as the control of “motivated behaviours”. The hypothalamus is also known as the arcuate nucleus (Arc). The two cells groups are called pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) cells. Scientists already knew that the Arc was involved in the ‘control of feeding’. Previous work had revealed that when receiving certain signals, POMC neurons act ‘like a break’ on eating and AgRP neurons act as the gas pedal – especially if it has been a while since the last meal.
The hypothalamus (red circle)
However, it was unclear how these two groups interacted with one an another. The investigators used a tool, called optogenetics, to map the mechanism’s signals by using laser light to activate and deactivate selective cells in the mice that were overeating. This revealed that when they activated the POMC, the AgRP cells were activated. Professor Akil explained that “When both are stimulated at once, AgRP steals the show.” Using another optogenetic method, scientists then found that they were able to activate the POMC cells without activating the AgRP cells, which lead to a significant decrease in the mice’s eating.
In a final set of experiments, the scientists revealed that activating AgRP also switches on the brain’s opioid system. Upon giving the mice the opioid receptor blocker naloxone, the feeding behaviour stopped. Professor Akil stated that “This suggests that the brain’s own endogenous opioid system may play a role in wanting to eat beyond what is needed”. Previous studies on this matter have shown that metabolic drivers of eating and overeating tend to focus on hormones, such as ghrelin ad leptin. However, this study has shown that the brain circuits, or neural systems, also play an important role. These could be reacting to emotional, social and perceptual signals.
Professor Akil urges scientists to further study this aspect of overeating as she says, “There’s a whole industry built on enticing you to eat, whether you need it or not, through visual cues, packaging, smalls, emotional associations. People get hungry just looking at them, and we need to study the neural signals involved in those attentional, perceptional mechanisms that drive us to eat”.