The next time you feel hungry even though you've already eaten a big meal, the culprit may be a certain protein. A new study shows that the protein AMPK regulates the neurons in the brain responsible for making you feel hungry. The findings may have implications in the treatment of obesity.

Researchers from Tufts University School of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School participated in the study that discovered a link between the protein and the neurons. The study indicates that the metabolic sensor protein AMPK activates agouti-related peptide (AgRP) neurons located in the brain's hypothalamus.

Researchers used mice to examine the role that the AMPK plays in the neurological behavior patterns of feeling hungry. They engineered some of the mice to continuously activate the AMPK protein whether or not they had been fed, and found these mice also had an increase in AgRP neuron activity, food consumption and weight gain. The mice with increased AMPK activity also showed an increase in the formation of AgRP dendritic spines, the membranous structures along neurons that receive synaptic inputs from other neurons.

The study additionally found that blocking a group of proteins called PAKs, known for causing the AMPK protein to activate, can have the opposite effect. Mice with blocked PAKs that had not been fed showed reduced AgRP neuron activity and dendric spine formation, even when AMPK remained in an active state.

It is not yet known how the protein and neurons communicate together to create feelings of hunger. Dong Kong, an assistant professor of neuroscience at Tufts University who authored the study, says further research is needed to understand the mechanisms that operate between AMPK, PAKs and AgRP neurons, and the signals produced by other key players in the metabolic process such as insulin, leptin and glucose.

"Given the wide expression of AMPK and PAK proteins, as well as other engaged molecules, our findings could have potentially broader effects on the study of synapse formation," Kong says. "While we do not provide a definitive target for drug development against obesity or eating disorders, we believe these findings clarify our understanding of this important energy-regulating pathway, and enable new approaches for future research and therapeutic studies."

This study comes on the heels of another study that also shed some new light on understanding the neurological behavior of hunger and how to combat it as obesity rates continue to climb. Researchers from Imperial College London and the University of Glasgow in Scotland released a new study earlier this week detailing a supplement that causes gut bacteria to release an appetite-suppressing propionate leading to decreases in appetite and weight gain.

The study was published in the journal Neuron.