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Have you ever eaten something, got sick and then you did not want to eat that food again because of how it made you feel? That is because a signal from the gut to the brain produced that sickness, thus creating a taste aversion. 

The conventional wisdom renders that there is one circuit in our brain that suppresses eating, it comes from the stomach and it makes you feel sick if you activate it too hard. Eating a portioned meal makes your body happy, though, even while you are stimulating a signal your brain to stop eating. This is according to Martin Myers Jr., M.D. Ph.D., the Michigan Diabetes Research Center's director. He said that there could be a circuit that can stop normal feeding without adverse effects. 

Now, a Cell Metabolism study may have discovered the second circuit in mice. The director of the Michigan Nutrition Obesity Research Center, Randy Seeley, Ph.D., together with Myers and other researchers sought to better understand which part of the brain curbs the appetite and which the neurons work on making mice want to eat more or not at all. 

The gut-brain signal that suppresses the appetite is triggered by a type of neuron, containing CALCR or calcitonin receptor, which lives in a structure of the hindbrain called the medulla. These neurons did not need to be active in the brain for gut sickness to cause an aversive response. 

Myers said that this study suggested that they might be able to dissociate the brainstem systems that stop feeding on those that cause nausea, and his group who found that they could genetically activate those CALCR neurons could do that. 

Singling out the responsible neuron

Since there are neurons that can suppress eating but can also cause aversive effects, that means that there are different types of neurons, or circuits, in the brain that can terminate feeding with differing emotional responses. When the researchers made adjustments and inactivated the neurons called CALCR, the researchers were taken aback when they made another discovery. It then contradicted the idea that the brain only controls short term meal sizes and consumption.  

By turning the neurons off, it did not only interfere with the suppression of feeding by gut signals, but it also caused an ongoing increase in food intake. The mice became obese, thus suggesting that the brainstem systems do not only control meal size, but the amount of food consumed long term. This created a predisposition to obesity because of the energy imbalance in the mice. 

Similarly, activating CALCR neurons decreased the food intake of the mice and the bodyweight without any aversive gut effects. In the research, Myers and fellow researchers found another neuron, called the CCK, and it also decreased food intake and body weight however it created an aversive internal response, not like the CALCR neurons. The difference between the two neurons, CCK and CALCR, was found in their circuits. 

Myers said that CCK activates what we would call a yucky circuit. The neurons activate a certain cell, the CGRP cells, which then create that sick feeling. Unlike CCK. activated CALCR neurons follow a yummy circuit, thus activating non-CGRP cells. 

Potential implications in humans

Obesity and being overweight affects more than one-third of the adult population in developed countries, which can then lead to diabetes or other serious health conditions such as heart disease, diabetes and more. 
Unfortunately, a lot of diet drugs work, but they make people feel nauseous after they take them Obesity is still one of the conditions that are difficult to manage pharmaceutically.

This is because the treatment options have limited therapeutic utility. A drug that turns on the CALCR and turns of the CGRP could benefit those who are suffering from obesity because it suppresses feeding and it creates a long term control of food intake and body weight. 

Myers also said that if they could figure out a drug for people with obesity that can suppress food intake to produce long term weight loss without the negative side effects, it could absolutely change people's lives.  

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