An international team of researchers has discovered a destructive mechanism related with leptin resistance leading to obesity. Independent fatty acids when elevated in the blood stream increases the presence of metabolites of fat in the brain. This in turn is found to interfere with leptin signaling that one should stop eating since the stomach is full.
In a new study, scientists fed mice with a diet containing high amount of fats and observed that MMP-2 enzyme was produced in its body, which has a negative effect on the receptors. This blocked the neuronal cell surface in hypothalamus in the brain. Due to the blockage of leptin binding with its receptors, the neurons do not receive any signal to stop eating. Scientists also showed that when MMP-2 is obstructed, the leptin can still signal hunger satisfaction by binding to its receptors. The research can have a broader scope in future if clinicians find out a solution to treating the leptin resistance by blocking MMP-2 in humans.
Researchers to Further Investigate Presence of Other Receptors
A team including researchers from the Tel Aviv University in Israel, Monash University in Australia, Salk Institute for Biological Studies in La Jolla, and University of California San Diego was formed and named “Mazor”. The researchers want to find out if there are other enzymes present to stimulate the hunger signal in the brain other than leptin and its receptors. The research work is published in the journal Science Translational Medicine on August 23 issue. Leptin resistance associated with obesity is a known process but the molecular process is not yet understood well.
In the days to come, researchers are aiming to design an inhibitor for the MMP-2 pathway to activate and then confirming the validity of the same mechanism in human cells. If there is a way to stop this protease activation then other membrane receptors may also be destroyed resulting in better therapies for managing worldwide obesity.