Neuroscientists from McGill University have discovered a group of nerve cells, which play a crucial role in the regulation of appetite and a tendency to obesity. NG2-glial cells proved to be responsible for the sense of satiety, and violation of the anticancer activity upon treatment enhances appetite.
The results are published in the journal Cell Metabolism.
About two decades ago, scientists discovered that the appetite is controlled by hormone leptin, which is produced by fat cells. It is delivered by the flow of blood into the brain, where it signals to certain centers of the latter that we are full and can no longer eat. Although leptin receptors have been found in the hypothalamus, it remains unknown how leptin affects food intake and weight.
In the new study, the researchers were able to answer this question. They drew attention to the cells in the median eminence of the hypothalamus, which are divided for most of life. The researchers used a special drug that contributes to the death of NG2-glial cells. It was found that without these experimental mice brain neurons can no longer receive signals from fat cells.
Three days after the start of the drug administration, some animals began to eat much more in large quantities than the control group of mice that did not receive the glial cell inhibitor. For 30 days their weight doubled: from 25 to 50 grams. Interestingly, other NG2-glial cells that were outside the midline elevation were not affected.
Scientists believe that there are hidden answer to the question why patients with brain cancer strangely tend to gain weight. Irradiation typically leads to suppression of glial cell division that leads to uncontrolled appetite. New techniques are directed at maintaining a population of neurons in the hypothalamus may help in the treatment of obesity.
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