The loss of appetite in patients with cancer in particular is explained by the action of a molecule of the immune system.
Why do we lose our appetite when we are sick? This question torments many of us. The answer: An immune system molecule interferes with areas of the brain responsible for regulating appetite. In study carried out by the Scripps Research Institute (IRST) in the United States, and published in the scientific journal The Journal of Neuroscience, researchers have discovered how a molecule activated by the immune system reduces the appetite of patients. This molecule, called interleukin 18, would hijack a circuit in the brain, altering the desire to eat.
A decrease associated with a risk of cachexia
As the study reminds us, a drop, or even a total loss, of appetite often leads patients to feel greater fatigue, and weakness in the face of the disease. “Treating loss of appetite does not cure an underlying disease, but it could help a patient cope,” said lead author of the study, Professor Bruno Conti, in a statement. Many times, loss of appetite can compromise clinical results. A weak individual is less likely to be able to cope with chemotherapy, for example. “.
As he explains, Professor Walter Francesconi, author of the study, has experienced this loss of appetite himself. While he was sick and hospitalized for about 20 days, in relatively serious condition, he ate less. Faced with this loss of appetite, his condition did not improve, and he lost almost 10kg. “When I got home, I was so weak that I couldn’t walk anymore,” he says.
Like the doctor, many patients regain their appetite when they recover. However, in patients with AIDS or cancer, the loss of appetite can turn into a disaster, causing cachexia, commonly referred to as “the second disease” by doctors. It causes a profound weakening of the organism, characterized by great fatigue, weight loss and muscle atrophy.
Interleukin interferes with areas of the brain
The study authors set out to understand how interleukin-18 works in the brain. Thanks to electrophysiological recordings, carried out on mice, they were able to demonstrate an effect of the molecule on a particular area of the brain: the nucleus of the terminal stria. This one is known to be involved in stress and anxiety reactions. The study showed that interleukin 18 in this region alters the secretion of GABA, a neurotransmitter that regulates appetite. “Interleukin 18 regulates food by directly blocking the mechanisms of the neural circuit”, explains Professor Bruno Conti. The researchers observed that the mice that were injected with interleukin ate significantly less than the other mice.
According to the researchers, this discovery could reorient the treatment of patients but also raise the possibility of intervening in the reduction of obesity in patients suffering from metabolic disorders.
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