Stress-level glucocorticoids increase fasting hunger and decrease cerebral blood flow in regions regulating eating.

Area of Science:

• Neuroendocrinology
• Metabolic Regulation
• Neuroimaging

Background:

• Appetite and energy homeostasis are regulated by neural pathways that overlap with stress neurobiology.
• Chronic stress can dysregulate the cortico-limbic striatal system, impairing the integration of homeostatic and hedonic food intake signals.
• Understanding stress-induced appetite alterations is crucial for addressing weight gain.

Purpose of the Study:

• To investigate the effects of glucocorticoids on metabolic, neural, and behavioral factors related to appetite and obesity risk.
• To determine how stress hormones influence brain activity and hunger signaling.

Main Methods:

• Randomized, double-blind, cross-over study involving overnight hydrocortisone or saline infusion.
• Fasting perfusion magnetic resonance imaging (MRI) to assess regional cerebral blood flow (CBF).
• Measurements included Visual Analog Scale (VAS) for hunger, cortisol, and metabolic hormones.

Main Results:

• Hydrocortisone infusion decreased CBF in the hypothalamus and cortico-striatal-limbic regions compared to saline.
• Hunger ratings, insulin, glucose, and leptin levels were significantly increased by hydrocortisone.
• Reduced CBF in specific brain areas (medial OFC, brainstem, thalamus) predicted increased hunger, which was associated with plasma insulin.

Conclusions:

• Glucocorticoid levels mimicking psychological stress increase fasting hunger.
• Decreased regional CBF in brain networks controlling food intake is observed.
• These findings link stress hormones, brain function, and appetite regulation, offering insights into obesity risk.