Eating when full: A battle between two brain signals


BEING overweight or obese increases the risk of developing several long-lasting conditions. Why does desire to keep eating overpower the signal that says we are full? New research discovers that it involves a struggle between two neighboring groups of brain cells in which the brain’s opioid system also has a role.
The study, which features in the Proceedings of the National Academy of Sciences, was carried out on mice, but the scientists believe that the findings will help us better understand similar mechanisms in humans,private channel reported “Our work,” explains senior study author Prof. Huda Akil, a neuroscientist in the Department of Psychiatry at the University of Michigan Molecular and Behavioral Neuroscience Institute in Ann Arbor, “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.”
Being overweight or obese increases the risk of developing several long-lasting conditions, such as cardiovascular diseases and type 2 diabetes, as well as cancer. Carrying too much weight is a worldwide public health problem, affecting low- and middle-income countries as well as high-income ones. World Health Organization (WHO) estimates from 2016 suggest that 39 percent of adults globally are overweight and 13 percent are obese. The pressure to better understand drivers of obesity such as the brain’s role in regulating eating has never been greater. Among these, note the study authors, are “the mechanisms that modulate both the initiation and the cessation of feeding.” Prof. Akil and her colleagues focused on two small groups of adjacent nerve cells, or neurons, in the hypothalamus, which is a small brain region that is involved in several functions, such as the control of “motivated behaviors.” The two cell groups are called pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) cells.
They reside in a region of the hypothalamus known as the arcuate nucleus (Arc). Scientists already knew that the two groups and the Arc were somehow involved in the “control of feeding.” Indeed, in previous work, some of the team had already revealed that on receipt of certain signals, POMC neurons act “like a brake” on eating and AgRP neurons act like the gas pedal — especially when a lot of time has elapsed since the last feed. What remained unclear, however, was how these two groups interacted.

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