Loss of appetite is a well-documented symptom of a number of illnesses and could leave you eating less. Now, a team of researchers has found why it happens.
The Scripps Research Institute (TSRI) scientists have discovered how an immune system molecule hijacks a brain circuit and reduces appetite. Their research points to potential targets for treating loss of appetite and restoring a patient’s strength.
“Treating loss of appetite won’t cure an underlying disease, but it could help a patient cope,” said senior author Bruno Conti. “Many times, loss of appetite can compromise clinical outcome. A weak individual is less likely to be able to cope with chemotherapy, for instance.”
On the flip side, the research also points to possible drug targets to reduce appetite and possibly support weight loss for those with metabolic disorders.
Previous studies had identified the biological players in loss of appetite. One was an immune molecule called interleukin 18 (IL-18), which activates other cells to fight disease. Another was a brain structure called the Bed Nucleus of the Stria Terminalis (BST), which has a subset of neurons that project to the Lateral Hypothalamus (LH), a brain region that controls appetite.
The new research began with the discovery of the expression of IL-18 receptors in neurons of the anterior BST. With this finding, the researchers had a starting point for tracking the effects of IL-18 in this part of the brain. The researchers believe the circuit affected by IL-18 may be a potential drug target for treating loss of appetite. They also brought up the possibility of intervening with a molecular mimic of IL-18 to control appetite and reduce obesity in patients with metabolic disorders.
Next up, the researchers plan to investigate the specific biochemical pathways in this brain circuit. The better they understand the pathway, the better targets they’ll have for potential therapies. The study appears in Journal of Neuroscience.