Brain Circuit Linking Stress to Blood Sugar Identified, Offering New Diabetes Insights
New York, NY - Researchers have pinpointed a direct neural pathway from the brain to the liver that rapidly elevates blood sugar levels in response to stress, a revelation published today in Nature. The finding challenges previous understandings of how stress impacts metabolic function and highlights a critical role for the amygdala in regulating physiological responses beyond behavior.
The study, conducted on mice, reveals that stress activates a circuit originating in the medial amygdala, triggering a cascade that ultimately instructs the liver to release sugar into the bloodstream within minutes. This immediate surge in blood glucose, while an ancient survival mechanism, can substantially increase the risk of developing type 2 diabetes with chronic or repeated stress exposure. An estimated 88.2 million U.S. adults – over 20% of the population – have prediabetes, a condition often preceding type 2 diabetes, according to the CDC. Understanding this brain-body connection could pave the way for novel interventions targeting stress-induced metabolic dysfunction.
“Our research doesn’t just change how we think about stress in relation to diabetes, but also about the importance of the amygdala,” explains Sarah Stanley, Assistant Professor at Mount Sinai and a led researcher on the project, in a press release. “Previously, we believed the amygdala primarily governed our behavioral stress response. Now we know this area also controls the physiological reaction. Stress has a huge impact on diabetes.”
The research team traced the pathway from the amygdala to the hypothalamus, and later to the liver. This circuit effectively overrides normal glucose regulation, prioritizing immediate energy availability - a response beneficial in acute, life-threatening situations, but detrimental when chronically activated.The study demonstrates a rapid and substantial increase in blood sugar levels in mice exposed to stressful stimuli.
This discovery opens avenues for exploring targeted therapies that could interrupt this stress-induced glucose release, potentially mitigating the long-term metabolic consequences of chronic stress. Further research will focus on validating these findings in humans and identifying potential pharmacological targets within the newly identified circuit.
