CALCR neurons may influence long-term control of food intake and body weight

CALCR neurons may influence long-term control of food intake and body weight

Reviewed by Kate Anderton, B.Sc. (Editor) Jan 17 2020 Ever eaten something, gotten sick and then didn't want to eat that food again because of how it made you feel? That's because a signal from the gut to the brain produced that sickness, creating a taste aversion. Conventional wisdom renders there's one circuit in the brain that suppresses eating -- it comes from the stomach and makes you feel sick if you activate it too hard. Eating a portioned meal makes your body happy, though, even while stimulating a signal to the brain to stop eating, according to Michigan Diabetes Research Center's director, Martin Myers Jr., M.D. Ph.D. "Therefore, there must be a circuit that stops normal feeding without the adverse effects, right?" says Myers. Now, a Cell Metabolism study may have discovered this second circuit in mice. Myers, Randy Seeley, Ph.D, the director of the Michigan Nutrition Obesity Research Center, and a team of researchers sought to better understand which part of the brain curbs appetite and which neurons play a role in making mice want to eat or not eat. The gut-brain signal that suppresses appetite is triggered by a type of neuron, containing calcitonin receptor (CALCR), which lives in a structure of the hindbrain called the medulla. Interestingly enough, these neurons didn't need to be active in the brain for gut sickness to cause an aversive response. "This suggested we might be able to dissociate the brainstem systems that stop feeding from those that cause nausea," says Myers, whose group found they could genetically activate those CALCR neurons to do just that. Singling out the responsible neuron Since there are neurons that can suppress eating but also cause aversive effects, that must mean there are different types of neurons, or circuits, in the brain that can terminate feeding with differing emotional responses. When the researchers inactivated the CALCR neurons, they were surprised to make another discovery, which contradicted the idea that the brain only controls short term meal sizes and consumption. Related Stories



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