Almost everyone feels that way. At a restaurant or a holiday meal, your stomach signals that youre full, so logically you should stop eating. But the food is so delicious, or your friends and family are still eating, so you havent stopped.
A new study by the Institute of Molecular and Neuroscience at the University of Michigan has been published in the Proceedings of the National Academy of Sciences. Researchers at the brain level have explored why this happens. By means of photogenetics, the researchers found that two small clusters of cells near the arcuate nucleus (the hypothalamus, the center of the regulation of motivational behavior) POMC (the "brake" in feeding behavior) and AgRP (the throttle in feeding behavior) control the competitive feeding behavior. When researchers used photogenetics to stimulate POMC cells, they inadvertently stimulated nearby AgRP cells, where signals from AgRP cells continue to feedbeat signals from POMC stop feeding. When both are stimulated, AgRP cells prevail. The research leader, neurologist Dr. Huda Akil said. The researchers then used another technique to expose POMC cells to photogenetic stimulation alone, and found that stimulating POMC cells alone significantly reduced feeding behavior, faster than expected.
The team also used a new method called CLARITY to display neural pathways starting with POMC and AgRP neurons in 3D. Once these neural pathways are activated, they will trigger the desire to feel satiety or to eat. They stitched together images of the activated neurons in the computer to create a 3-D video showing the range of activity of the neurons. Then, the researchers used a method called c-fos to study the downstream effects of POMC and AgRP neurons activation, which spread throughout the brain, including the cortex that controls attention and memory.
Since POMC encodes a natural opioid (b-endorphin), researchers wonder whether activating the system triggers the bodys own natural opioid system, the endogenous opioid system. They found that activation of POMC blocked pain, but naloxone, an opioid antagonist, reversed the effect. Interestingly, feeding triggering activity also activates opioid systems in the brain. When we use naloxone, which blocks opioid receptors, the feeding behavior stops. This suggests that the brains own endogenous opioid system may play a role in binge eating, Akil said.
Because of the involvement of the cortex and the opioid system, Akil and her colleagues began to think about the relationship between these results and human experience. Although mice are very different from humans, Akil speculates that our senses are impacted by food-related vision and smell, as well as by food-related social interactions, and perhaps these factors combine to make us interested in eating when we are not hungry.
Our research suggests that the signals of satiety are not strong enough to counteract the strong desire to eat, and that desire is of great evolutionary value. Many studies in humans have focused on the metabolic aspects of diet and overeating for example, the metabolic signals that are transmitted between the body and the brain in the form of polypeptides such as leptin and ghrelin, she said. But there seems to be a powerful nervous system involved in binge eating, which is caused by perceptual, emotional and social factors and does not receive enough scientific attention.
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