When fasted mice were re-fed, activating AgRP neurons prevented the expected increase in monocyte levels, indicating that the brain's perception of hunger can influence immune responses.

Dr. Giuseppe D'Agostino, the study's lead researcher, emphasized that these findings highlight the brain's significant role in regulating immune function, underscoring the importance of the mind-body connection.

Researchers from the University of Manchester investigated whether the immune regulation observed during fasting is influenced by direct nutrient sensing or requires signaling from the brain.

Their study, published in Science Immunology, reveals that fasting-induced immune changes can be replicated by activating specific neurons in the hypothalamus.

While fasting is known to lower inflammation and reduce pro-inflammatory monocytes, the precise mechanisms behind these immune reorganizations remain unclear.

The study found that activating AgRP neurons in mice decreased circulating pro-inflammatory monocytes, mimicking the effects of a 20-hour fast without lowering blood glucose levels.

Conversely, activating pro-opiomelanocortin (POMC) neurons in fasted mice led to an increase in monocyte numbers, reversing the effects of fasting despite the absence of food.

The research indicates that hepatic mTOR activity, a crucial regulator of longevity, is influenced by neuronal signals from AgRP and POMC neurons, independent of local nutrient levels.

The activation of AgRP neurons also resulted in decreased levels of the cytokine CCL2, which is responsible for recruiting monocytes from the bone marrow, further linking neuronal activity to immune regulation.

These findings have important implications for treating infections, malnutrition, and cancer-related muscle wasting, suggesting potential health benefits associated with fasting.