Theobesitythe world does not stop growing, and the main cause is excessive food intake. In a study of the brain circuits that control hunger and satiety, researchers at the Yale University School of Medicine (USA) have concluded thatthe molecular mechanism that regulates free radicals also plays a key role in increasing appetite. As revealed in a study published inNature Medicine, the increase of free radicals in thehypothalamusthe brain region of the brain that controls body temperature, sleep, hunger and thirstsuppresses appetite in obese miceactivating satiety neurons, secreting melanocortin. The bad thing isfree radicals also accelerate aging. ? On the one hand, we need them to stop eating. On the other hand, if we expose ourselves chronically, they damage cells and accelerate aging ?, explains David W. Wallace, co-author of the work.
In their experiments with mice, the scientists observed that, after eating, the neurons responsible for excessive ingestion had high levels of free radicals. This process is driventhe hormone leptin and glucose, sending signals to the brain to modulate food intake. When the mice eat, the levels of leptin and glucose go up, as well as levels of free radicals. However, in mice with diet-induced obesity, these same neurons reduced this activity (leptin resistance); in these mice, the levels of free radicals were dampened by peroxisomes, preventing the activation of these neurons and, therefore, the ability to feel satiated after eating.
